Curcumin has been shown to inhibit renal fibrosis, but whether curcumin mediates renal fibrosis progression by regulating the circular RNA (circRNA)-related pathway remain unclear.

TGF-β1 was used to construct renal injury and fibrosis cell model. Cell growth was evaluated by cell counting kit 8 assay, EdU assay and flow cytometry. Fibrosis marker and interleukin 6 signal transducer (IL6ST) protein levels were measured using western bolt analysis. Inflammation factor concentrations were determined by ELISA. Circ_0008925, miR-204-5p and IL6ST expression was assessed by qRT-PCR. Unilateral ureteral obstruction (UUO) mice models were constructed to assess the role of curcumin in vivo.

Curcumin treatment alleviated TGF-β1-induced HK-2 cell apoptosis, inflammation and fibrosis in vitro, as well as relieved renal injury in UUO mice models in vivo. Circ_0008925 was highly expressed in TGF-β1-induced HK-2 cells and its expression was inhibited by curcumin. Circ_0008925 could sponge miR-204-5p to positively regulate IL6ST. The inhibition effect of curcumin on TGF-β1-induced HK-2 cell injury and fibrosis was reversed by circ_0008925 overexpression, miR-204-5p inhibitor or IL6ST upregulation. Besides, circ_0008925 knockdown inhibited TGF-β1-induced HK-2 cell injury and fibrosis by suppressing IL6ST expression.

Curcumin relieved renal fibrosis through regulating circ_0008925/miR-204-5p/IL6ST axis.

Human serum albumin (HSA) plays an indispensable role as a carrier of endogenous and exogenous substances in vivo. The efficiency of endocytosis determines the transport capacity. However, the potential for enhancing the efficiency of HSA endocytosis remains largely unknown. This research represented a substantial advancement, revealing that Fe2+ markedly increased HSA endocytosis. Moreover, Fe2+ facilitated the endocytosis and transport of HSA in vivo. The enhancement in HSA uptake facilitated by Fe2+ is markedly decreased following iron chelation, indicating a specific interaction between Fe2⁺ and HSA that promoted endocytosis. Moreover, the study elucidated that FcRn and caveolin regulated HSA endocytosis under normal conditions. Yet, in the presence of Fe2⁺, endocytosis shifted toward clathrin- and caveolin-enriched membrane domains, requiring both divalent metal transporter 1 (DMT1) and FcRn for efficient process completion. Thereby a new pathway is discovered for Fe2+-dependent HSA endocytosis involving DMT1 and clathrin. This findings highlighted the crucial role of iron in enhancing HSA endocytosis and transport, establishing Fe2+ as a vital endocytic enhancer that required binding to HSA to substantially improve its uptake. This insight into the mechanism of HSA endocytosis not only expands the understanding of protein transport but also opens new avenues for therapeutic intervention.

In this study the wound healing efficacy of new self-assembling curcumin loaded nanohyaluronan-glycerosomes has been tested in healthy and diabetic rats. Curcumin was loaded in nanohyaluronan-liposomes and -glycerosomes, special vesicles obtained mixing curcumin, hyaluronan nanohydrogel and soy lecithin. Curcumin loaded liposomes and glycerosomes were also prepared, characterized and tested as references. The physico-chemical (size and size distribution, surface charge and morphology), and technological (entrapment efficiency, stability over time and skin delivery) characteristics and biological performances (safety, ability to protect in vitro cells from oxidative damage) of prepared formulations were measured. Finally, they were daily applied to skin wounds of healthy or diabetic rats. The animal skin was excided and analysed at days 3, 7 and 14. The macroscopic observation underlined the higher ability of curcumin loaded nanohyaluronan-glycerosomes to improve wound healing in diabetic rats, already on day 3 up to day 14 (p < 0.05). Histopathological analysis confirmed an accelerated re-epithelization in healthy rats, while increased angiogenesis in diabetic ones. The superior therapeutic efficacy of curcumin loaded nanohyaluronan-glycerosomes compared to other formulations can be related to their enhanced ability to deliver higher curcumin concentrations at the wound site due to a synergistic effect of glycerol, hyaluronan nanohydrogel and lecithin.

Aging is a complex phenomenon involving oxidative stress, inflammation, and cellular damage subsequently leading to various disorders, such as cardiovascular diseases, neurodegenerative disorders, diabetes, and cancer. Sirtuin (SIRT) proteins are one of the major molecular factors that affect human aging. Sirtuins are a class of NAD+-dependent enzymes that control oxidative stress response, DNA damage repair, inflammation and metabolism, all of which are involved in aging and age-related diseases.

The objective of this review is to elucidate the potential role of SIRT in the aging process and modulation of SIRT pathway through selected phytochemicals like Curcumin, Resveratrol, Quercetin, and Kaempferol.

Studies convincedly revealed that SIRT pathway represents a promising avenue for extending the human health span and addressing age-related conditions. Phytochemicals like Curcumin, Resveratrol, Quercetin, and Kaempferol have shown excellent potential to mediate aging effects through their potent antioxidant, anti-inflammatory, and regulatory activities. These potent bioactive compounds enhance oxidative stress response, genomic integrity, neuroprotective and anti-inflammatory activities through SIRT pathway modulation. Furthermore, in addition to antiaging effects, other therapeutic benefits are also associated with each compound including nervous disorders, cancer, and metabolic disorders are also briefly highlighted. Studies reported convincing evidence that Curcumin, Resveratrol, Quercetin, and Kaempferol, effectively modulate SIRT expression/activity leading to improved cell stress tolerance, reduced oxidation and enhanced metabolic state.

Collectively, studies revealed the comprehensive nutraceutical significance of Curcumin, Resveratrol, Quercetin, and Kaempferol as anti-aging therapeutics and warrant future studies to exploit the full potential of these natural compounds.

Cardiovascular disorders (CVDs) are the leading cause of mortality worldwide, highlighting an urgent need for innovative therapeutic strategies. Recent advancements highlight the potential of naturally derived bioproducts with epigenetic properties to offer protection against CVDs. These compounds act on key epigenetic mechanisms, DNA methylation, histone modifications, and non-coding RNA regulation to modulate gene expression essential for cardiovascular health. This review explores the effects of various bioproducts, such as polyphenols, flavonoids, and other natural extracts, on these epigenetic modifications and their potential benefits in preventing and managing CVDs. We discuss recent discoveries and clinical applications, providing insights into the epigenetic regulatory mechanisms of these compounds as potential epidrugs, naturally derived agents with promising therapeutic prospects in epigenetic therapy for CVDs.

Non-small cell lung cancer (NSCLC) poses a significant threat to public health worldwide. Curcumae Rhizoma (CR) has potent therapeutic potential in different cancers. However, the mechanism of CR treating NSCLC remains unclear. In this study, a network pharmacology-based strategy is followed to address the issue. The targets related to CR or NSCLC were obtained from multiple online public databases. Compound-target network was constructed using Cytoscape. Protein-protein interaction (PPI) was analyzed by STRING. Key transcription factors were explored in TRRUST. Gene ontology (GO) function and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analysis were accomplished in Metascape. The druglikeness of compounds was tested in Molinspiration Cheminformatics Software. Autodock Vina was used for molecular docking. Molecular dynamic (MD) simulation was performed using Gromacs. There were 104 overlapped targets considered as key targets of CR treating NSCLC. The key components of CR, including reynosin, (4S,5S)-13-hydroxygermacrone 4,5-epoxide, and (E)-1,7-bis(4-hydroxyphenyl)-6-hepten-3-one, were screened by topological parameters and bioactivity scores. Central clustered targets in PPI network (epidermal growth factor receptor [EGFR], SRC, JAK2, and mitogen-activated protein kinase 3 [MAPK3]) were identified as critical therapeutic targets of CR. GO and KEGG enrichment analysis suggested that therapeutic effect of CR on NSCLC involved various biological processes, cellular components, and molecular functions, and pathways in cancer, JAK-STAT signaling pathway, and p53 signaling pathway were strongly related. Molecular docking and MD simulation suggested that key compounds in CR had high binding affinity to critical NSCLC targets, like EGFR, JAK2, SRC, and MAPK3, with stable complexes formed. This study revealed key components and mechanism of CR treating NSCLC based on a network pharmacology-driven strategy, providing a reference for in-depth study on treating NSCLC.

Nonalcoholic fatty liver disease (NAFLD) is a growing global health concern, impacting approximately 32.4% of the worldwide population. As a disease linked to metabolic dysfunction, NAFLD continues to rise alongside global increases in obesity, type 2 diabetes mellitus (T2DM), and metabolic syndrome. There is considerable evidence indicating that NAFLD disproportionately affects racial, ethnic, and minority groups, although the exact reasons for these disparities remain elusive. Contributing factors to this disease may include socioeconomic status, cultural influences, stress, genetic factors, and lifestyle choices. Emerging evidence suggests that these causal factors could influence epigenetic mechanisms, particularly DNA methylation and histone modifications, as well as the composition and diversity of gut microbiota. Nevertheless, there is a scarcity of research that comprehensively examines the interplay between epigenetic changes and gut microbiome variations in relation to NAFLD disparities across different racial and ethnic populations globally. This paper intends to (i) explore the connections between NAFLD, ethnic disparities, gut microbiota composition, and epigenetic alterations, while reviewing pertinent studies that illustrate how these factors contribute to health inequities among various ethnic groups impacted by this disease; (ii) explore potential therapeutic targets and biomarkers to advance the management of NAFLD; and (iii) provide insights to enhance our understanding of the mechanisms associated with this disease, thereby promoting further research in this field. Advancements in this area are anticipated to enhance our understanding of disease susceptibilities in at-risk groups and to provide new therapeutic options for NAFLD and its associated complications.

Oral squamous cell carcinoma (OSCC) is one of the most common malignant tumors of head and neck with high incidence and poor prognosis. Curcumin, as a drug-food congener, has a broad spectrum of anticancer effects, and based on this property, we further focused on EF24, a small molecule compound using curcumin as a backbone, to study the effects of both in OSCC.

Cell experiments were performed to test the inhibitory effect of curcumin and EF24 on OSCC cells. The potential mechanism was further analyzed by transcriptome sequencing, and the DEGs after drug treatment were determined. PPI networks were created using Cytoscape software.

Both curcumin and EF24 inhibit the viability, migration, and invasion, and induce apoptosis of OSCC cells and the IC50 of EF24 was much lower than that of curcumin. Analysis of DEGs identified 893 DEGs following curcumin treatment, of which 794 were up-regulated and 99 were down-regulated; 797 DEGs following EF24 treatment were identified, of which 665 were up-regulated and 132 were down-regulated. Curcumin and EF24 were found to down-regulate lipid metabolism by key enzymes that regulate fatty acid and cholesterol synthesis. Furthermore, the number of T cell CD4 + memory is up-regulated and the immune response is enhanced.

It is suggested that curcumin and EF24 inhibit the metabolic reprogramming of tumor cells and at the same time regulate TME, and improve the immunotherapy of tumors, which opens the way for the future treatment of OSCC with this approach alone or in conjunction with immune-checkpoint blocking.

Curcumin has diverse biological functions, especially antioxidant and anti-inflammatory properties, but clinical trials have been hindered by its low bioavailability and pharmacokinetic properties. To achieve therapeutic efficacy, understanding curcumin's in vivo metabolism is crucial. We reviewed current research on curcumin metabolism in PubMed, Google Scholar, and CNKI. This article outlines curcumin's metabolic processes in the body via oral and intravenous injection. It suggests that upon entering the human body, curcumin may undergo oxidation, reduction, binding, and microbial community influence.

The kidney is frequently exposed to high levels of drugs and their metabolites, which can injure the kidney and the proximal tubule (PT) in particular. In order to detect nephrotoxicity early during drug development, relevant in vitro models are essential. Here, we introduce a robust and versatile cell culture insert-based iPSC-derived PT model, which can be maintained in a microphysiological system for at least ten days. We demonstrate the model's ability to predict drug-induced PT injury using polymyxin B, cyclosporin A, and cisplatin, and observe that perfusion distinctly impacts our model's response to xenobiotics. We observe that the upregulation of metallothioneins that is described in vivo after treatment with these drugs is reliably detected in dynamic, but not static in vitro PT models. Finally, we use our model to alleviate polymyxin-induced nephrotoxicity by supplementing the antioxidant curcumin. Together, these findings illustrate that our perfused iPSC-derived PT model is versatile and well-suited for in vitro studies investigating nephrotoxicity and its prevention. Reliable and user-friendly in vitro models like this enable the early detection of nephrotoxic potential, thereby minimizing adverse effects and reducing drug attrition.

Polymer nanoparticle-based drug carriers represent a new avenue for cancer therapy. In this work, we study the formation of chitosan/lignin (Chi/Lig) core-shell particles doped with samarium oxide nanoparticles as potential carriers for the hydrophobic anticancer drug curcumin. Electrostatic coassembly was responsible for the formation of Chi/Lig core-shell particles. The structural characterization suggested interactions between chitosan, lignin, and Sm2O3 through electrostatic interactions, such as hydrogen bonding. The incorporation of lignin into the chitosan matrix results in the formation of an amphiphilic core-shell structure, offering the potential for dual-drug-loading strategy studies, wherein one hydrophobic drug could reside in the lignin core while another hydrophilic drug occupies the chitosan shell. Additionally, the incorporation of lignin into the polymer systems not only contributes to a slower release of curcumin but also enables the design of pH-responsive drug carriers. Moreover, the strong red fluorescence observed in the samarium-containing composites suggests their potential for applications in bioimaging and in vitro assays, particularly with orally delivered microcarriers.

Developing treatments for age-related diseases requires cost-effective and efficient approaches. Nutrients and natural metabolites offer safer alternatives to synthetic drugs. Aging increases the need for solutions that protect health and repair cells. Recent studies show that nutrients and natural products reduce oxidative stress, regulate metabolism, and influence longevity-related genes. This review focuses on vitamins, minerals, antioxidants, and natural products that improve healthspan and combat aging. It also discusses challenges such as standardization, clinical validation, and regulatory approval. Finally, emerging trends, such as personalized nutrition and advanced delivery systems, highlight the potential of these metabolites for addressing aging.

Liquid-liquid phase separation (LLPS) is a significant reversible and dynamic process in organisms. Cells form droplets that are distinct from membrane-bound cell organelles by phase separation to keep biochemical processes in order. Nevertheless, the pathological state of LLPS contributes to the progression of a variety of tumor-related pathogenic issues. Sarcoma is one kind of highly malignant tumor characterized by aggressive metastatic potential and resistance to conventional therapeutic agents. Despite the significant clinical relevance, research on phase separation in sarcomas currently faces several major challenges. These include the limited availability of sarcoma samples, insufficient attention from the research community, and the complex genetic heterogeneity of sarcomas. Recently, emerging evidence have elaborated the specific effects and pathways of phase separation on different sarcoma subtypes, including the effect of sarcoma fusion proteins and other physicochemical factors on phase separation. This review aims to summarize the multiple roles of phase separation in sarcoma and novel molecular inhibitors that target phase separation. These insights will broaden the understanding of the mechanisms concerning sarcoma and offer new perspectives for future therapeutic strategies.

Lung cancer, particularly NSCLC, poses a major therapeutic challenge due to drug resistance and the poor aqueous solubility of chemotherapeutic agents, limiting treatment efficacy. This study investigates inhalable micelles for the codelivery of curcumin (CUR) and icariin (ICA), two hydrophobic bioactive compounds with anticancer potential, as a targeted therapeutic approach for NSCLC. The optimized micellar formulation (9:1 TPGS/DPPC) yielded nanomicelles (∼18 nm) with high encapsulation efficiency (∼90%) and a zeta potential of -1.24 mV, demonstrating stability for pulmonary administration. In vitro cytotoxicity studies demonstrated enhanced anticancer activity of CUR- and ICA-loaded micelles against A549 lung cancer cells (IC50 = 3.0 μg/mL), lower than doxorubicin (30 μg/mL), suggesting enhanced cytotoxic potential. Additionally, DPPH assays confirmed that encapsulation preserved curcumin's functionality. Aerosolization studies demonstrated a high fine particle fraction (67 ± 3%) and emitted fraction (95 ± 1.0%), confirming the micelles' suitability for deep lung deposition and effective pulmonary drug delivery. These findings highlight the potential of CUR- and ICA-loaded micelles as an inhalable NSCLC treatment, requiring further preclinical investigation.

Curcumin (CUR), a bioactive compound found in turmeric, has garnered attention for its potential anti-inflammatory properties and impact on liver health. Numerous studies suggest that CUR may be crucial in mitigating liver inflammation. The compound's anti-inflammatory effects are believed to be attributed to its ability to modulate various molecular pathways involved in the inflammatory response. Research indicates that CUR may suppress the activation of inflammatory cells and the production of pro-inflammatory cytokines in the liver. Additionally, it has been observed to inhibit the activity of transcription factors that play a key role in inflammation. By targeting these molecular mechanisms, CUR may help alleviate the inflammatory burden on the liver. Moreover, CUR's antioxidant properties are thought to contribute to its protective effects on the liver. Oxidative stress is closely linked to inflammation, and CUR's ability to neutralize free radicals may further support its anti-inflammatory action. While the evidence is promising, it is essential to note that more research is needed to fully understand the precise mechanisms through which CUR influences liver inflammation. Nevertheless, these findings suggest that CUR could be a potential therapeutic agent in managing liver inflammatory conditions. In this review, we explore the potential impact of CUR on inflammation, highlighting the key mechanisms involved, as reported in the literature.

Huntington's disease (HD) is a neurodegenerative disorder in which mutated fragments of the huntingtin protein (Htt) undergo misfolding and aggregation. Since aggregated proteins can cause cellular stress and cytotoxicity, there is an interest in the development of small molecule aggregation inhibitors as potential modulators of HD pathogenesis. Here, we study how a polyphenol modulates the aggregation mechanism of huntingtin exon 1 (HttEx1) even at sub-stoichiometric ratios. Sub-stoichiometric amounts of curcumin impacted the primary and/or secondary nucleation events, extending the pre-aggregation lag phase. Remarkably, the disrupted aggregation process changed both the aggregate structure and its cell metabolic properties. When administered to neuronal cells, the 'break-through' protein aggregates induced significantly reduced cellular stress compared to aggregates formed in absence of inhibitors. Structural analysis by electron microscopy, small angle X-ray scattering (SAXS), and solid-state NMR spectroscopy identified changes in the fibril structures, probing the flanking domains in the fuzzy coat and the fibril core. We propose that changes in the latter relate to the presence or absence of polyglutamine (polyQ) β-hairpin structures. Our findings highlight multifaceted consequences of small molecule inhibitors that modulate the protein misfolding landscape, with potential implications for treatment strategies in HD and other amyloid disorders.

In 2015, the United Nations officially launched the Sustainable Development Goals (SDGs) as "the blueprint to achieve a better and more sustainable future for all. They address the global challenges we face, including those related to poverty, inequality, climate change, environmental degradation, peace and justice. The 17 Goals are all interconnected, in order to leave no one behind, it is important that we achieve them all by 2030". Here, we have embedded medicinal chemistry as a key player to achieve SDGs. We firmly believe that medicinal chemistry can and must contribute to a sustainable future and a better world with an improved quality of life for all. We have taken a critical look at each of the SDGs, dividing them into Priority and Foundational, and analyzed how medicinal chemistry has an impact on each of them. Although much has been done, we are determined to make progress in this area.

Hydroxysafflor yellow A (HSYA) possesses a variety of pharmacological activities which has been demonstrated to be effective against ischemic heart disease (IHD). This study aimed to comprehensively examine the efficacy and summarize the potential mechanisms of HSYA against IHD in animal models.

We conducted electronic searches for preclinical studies on PubMed, Embase, Web of Science, Cochrane Library, CNKI, SinoMed, Wanfang, and Chinese VIP databases from inception to 31 January 2024. The CAMARADES checklist was chosen to assess the quality of evidence. STATA 14.0 software was utilized to analyze the data. The underlying mechanisms were categorized and summarized.

Twenty-eight studies involving 686 rodents were included and the mean score of methodology quality was 5.04 (range from 4 to 7). Meta-analysis observed that HSYA could decrease myocardial infarction size (SMD: -2.82, 95%CI: -3.56 to -2.08, p < 0.001) and reduce the levels of biomarkers of myocardial injury including cTnI (SMD: -3.82, 95%CI: -5.20 to -2.44, p < 0.001) and CK-MB (SMD: -2.74, 95%CI: -3.58 to -1.91, p < 0.001). HSYA displayed an improvement in cardiac function indicators including LVEF, LVSP, +dp/dt max and -dp/dt max. Furthermore, HSYA was able to reduce the levels of MDA, TNF-α and IL-6, while increasing SOD and NO levels. Mechanistically, the protective effect of HSYA in alleviating myocardial injury after ischemia may be associated with NLRP3 inflammasome, Bcl-2, Bax, caspase-3, eNOS proteins, and TLR/NF-κB, Nrf2/HO-1, JAK/STAT, PI3K/Akt, AMPK/mTOR, VEGFA pathways.

This study demonstrates that HSYA exerts cardioprotective effects in decreasing infarct size, reducing myocardial enzymes and improving cardiac function, which may be mediated by anti-inflammatory, antioxidant, anti-apoptotic, regulation of autophagy, improvement of microcirculation and promotion of angiogenesis. However, the absence of safety assessment, lack of animal models of co-morbidities, and inconsistency between timing of administration and clinical practice are limitations of preclinical studies.

clinicaltrials.gov, Identifier, CRD42023460790.

Curcumin is a natural polyphenol extracted from plants that can interact with various molecular targets, including antioxidant, antibacterial, anticancer, and anti-aging activities. Due to its variety of pharmacological activities and large margin pf safety, curcumin has been used in the prevention and treatment of various diseases, such as Alzheimer's, heart, and rheumatic immune diseases. To develop curcumin eye drops that can be used as antioxidant and antibacterial agents after phacoemulsification, we have designed a nano-based drug delivery system to improve curcumin bioavailability and duration of action. We successfully prepared zeolitic imidazolate framework-8 (ZIF-8) coated with chitosan-liposome (Cur@ZIF-8/CS-Lip) for curcumin delivery. It can release curcumin for over 20 hin vitroand exhibits excellent biosafety, antioxidant, and antibacterial activities. Therefore, we hypothesized that Cur@ZIF-8/CS-Lip could reduce the incidence of oxidative stress and infection after cataract surgery.

Deoxynivalenol (DON) is a pervasive ribotoxic stressor that induces intestinal epithelial barrier disruption by impairing tight junctions (TJs) and causing cellular damage. Curcumin (CUR), known for its enteroprotective properties and low toxicity, has been shown to attenuate DON-induced intestinal epithelial barrier injury. However, the underlying mechanisms are still unclear. In this study, we established in vivo and in vitro models using 30 male Kunming mice and IPEC-J2 cells to investigate the mechanisms by which CUR alleviates DON-induced intestinal epithelial barrier injury. The results showed that CUR markedly reduced DON-induced increases in intestinal permeability by restoring TJ protein expression (Claudin-4 and occludin) and preventing fiber-shaped actin (F-actin) contraction. CUR also attenuated DON-induced apoptosis by downregulating p53 and caspase activation and alleviated the G1 cell cycle arrest by reducing p21 expression. Mechanistically, CUR inhibited the activation of the ribosomal stress response (RSR)-associated p38 pathway, evidenced by decreased phosphorylation of p38, GSK3β, and ATF-2. The p38 activator dehydrocorydaline reversed CUR's protective effects. In conclusion, CUR alleviates DON-induced intestinal epithelial barrier disruption by improving RSR-associated p38 pathway-mediated TJ injury, apoptosis, and cell cycle arrest. These findings highlight the potential of CUR as a therapeutic agent for mitigating mycotoxin-induced intestinal dysfunction and suggest new avenues for drug target discovery.

Atherosclerosis (AS) is a major contributor to cardiovascular diseases, characterized by high morbidity and mortality rates. Long non-coding RNAs (LncRNAs), as members of non-protein coding RNAs, play a crucial role in various biological processes that maintain homeostasis and influence disease progression. Research indicates that lncRNAs are involved in the pathogenesis of AS.

In this study, we aim to explore the role of lncRNAs in the pathogenesis of AS and the latest progress in the prevention and treatment of AS by targeted regulation of lncRNAs by traditional Chinese medicine (TCM), in order to provide more new beneficial targets for the treatment of AS and expand the application of TCM in the treatment of cardiovascular diseases.

The literature was retrieved, analyzed, and collected using PubMed, Web of Science, Sci-Hub, CNKI, Elsevier, ScienceDirect, SpringerLink, and Google Scholar. Search terms include "atherosclerosis", "traditional Chinese medicine", "natural products", "active ingredient", "lncRNAs", "herbal medicine", "cardiovascular diseases", "pharmacology", "toxicology", "clinical trials", etc., and several combinations of these keywords.

This study examines the primary mechanisms through which lncRNAs induce AS, such as dysfunction in endothelial cells, abnormal proliferation of vascular smooth muscle cells, cholesterol buildup in macrophages, formation of foam cells, inflammatory responses, and imbalances in lipid metabolism. Additionally, it summarizes 16 herbal monomers and 6 Chinese herbal compounds, along with an analysis of the toxicological aspects of TCM.

The study explores the existing approaches for modulating lncRNAs and emphasizes the significance and potential of herbal monomers, extracts, and formulations in this context.

The application of natural products for cancer treatment has a long history. The safety and multifunctionality of naturally occurring substances have made them appropriate for cancer treatment and management. Curcumin affects multiple molecular pathways and is advantageous for treating both hematological and solid tumors. Nonetheless, the effectiveness of curcumin in vivo and in clinical studies has faced challenges due to its poor pharmacokinetic profile. Consequently, nanoparticles have been developed for the administration of curcumin in cancer treatment. The nanoparticles can enhance the distribution of curcumin in tissues and increase its therapeutic effectiveness. Furthermore, nanoparticles expand the uptake of curcumin in cancer cells, leading to increased cytotoxicity. Carbohydrate polymer-based nanoparticles provide a promising solution for the delivery of curcumin in cancer treatment by addressing its low solubility, limited bioavailability, and quick degradation. These biodegradable and biocompatible carriers, originating from polymers such as chitosan, hyaluronic acid, and alginate, protect curcumin, improving its stability and allowing for controlled release. Targeting ligands for functionalization provides selective and specific distribution to the tumor cells, enhancing therapeutic effectiveness and reducing off-target impacts. Their capacity to encapsulate curcumin with other agents allows for synergistic therapies, enhancing anticancer results even more. The adjustable characteristics of carbohydrate nanoparticles, along with their minimal toxicity, develop a revolutionary, functional and safe platform.

Curcumin is recognized for its diverse biological activities, including the ability to induce apoptosis and ferroptosis. Therefore, it represents a promising candidate for the development of new compounds with neuroprotective and anticancer properties. In order to synthesize mimics with improved pharmacokinetic properties (better solubility and stability than curcumin) here, we present the design and synthesis of novel curcumin analogues named Ethylphosphonate-based curcumin mimics (EPs), which preserve the pharmacophoric features of curcumin. New EP mimics were synthesized by tyrosol- and melatonin-based building blocks using an orthogonal protection approach of the different precursors' OH functions with good yields and in a few steps. Comparative screenings of the cytotoxic and cytoprotective properties (curcumin was used as a reference compound) were carried out on all new mimics in different cell lines (HeLa, A375, WM266, MDA-MB-231, LX2, and HDF). Assays with inhibitors of ferroptosis (Ferrostatin-1, Fer-1) and apoptosis (Quinoline-Val-Asp-difluorophenoxymethyl ketone, Q-VD), in combination with curcumin, suggested the specific cell death pathway (apoptotic or ferroptotic) of EPs, depending on the aromatic moieties contained in them. Interestingly, EP4 exhibited substantial cytotoxic effects against various human cancer cell lines (HeLa, A375, WM266) while sparing normal cells (HDFs). EP4 displayed a five-times-higher toxicity in triple-negative MDA-MB-231 and LX2 stellate cells than curcumin. The cytotoxicity exerted by EP4 involves only an apoptotic mechanism, contrary to curcumin, which exerts both apoptotic and ferroptotic effects. Additionally, EP4 was also found to be a very potent inhibitor of the ubiquitin-activating enzyme E1, reinforcing the anticancer potential of this compound. Furthermore, EP2 possesses high antioxidant properties, efficiently protects against cell death by ferroptosis, and inhibits the amyloid aggregation involved in AD.

Curcumin has a clear immunopharmacological effect and plays an important role as an immune agent in various immune diseases and tumor immunotherapy. To comprehensively and scientifically clarify and reflect the development process, current status, and research trends of curcumin in the field of immune regulation, and to provide reliable insights for discipline development strategies and future research expansion, this study systematically analyzes 3939 valid articles related to curcumin and immunity published between 2004 and 2024 from the Web of Science database. Using Citespace and R-bibliometrix software for bibliometric analysis, we create visual knowledge maps from multiple dimensions including overall publication output, influential research entities, highly cited papers, research topics and hotspots. The results indicate that the overall number of publications and citations is currently in a rapid development phase. China occupies a core position in this research field but has low collaboration intensity. The Egyptian Knowledge Bank (EKB) is the institution with the highest publication volume. Moreover, cluster analysis reveals that research hotspots are gradually shifting from fundamental pathology to topics involving broad social and environmental influences. The top five keywords with the most explosive citations-curcumin, inflammation, apoptosis, oxidative stress, and cancer-represent the most focused and influential research topics. Currently, curcumin immunology has developed a diversified research perspective, accumulating significant research in the areas of active substance basis, pharmacological activity, anti-inflammatory, and anti-cancer studies. The thematic evolution trends and keywords related to curcumin's immunological mechanisms summarized in this article provide insights and guidance for future research directions.

Background/Objectives: HIV persists in central nervous system (CNS) reservoirs, where infected microglia and macrophages drive neuroinflammation, oxidative stress, and neuronal damage, contributing to HIV-associated neurocognitive disorder (HAND). Nanoparticle-based drug delivery systems, particularly poly(lactic-co-glycolic acid) (PLGA) nanoparticles, offer a promising strategy to improve CNS antiretroviral therapy (ART) delivery. This study aimed to evaluate the efficacy of co-administration of PLGA nanoparticles (NPs) encapsulating elvitegravir (EVG) and curcumin (CUR) in targeting CNS reservoirs, reducing neuroinflammation, and mitigating oxidative stress. Methods: PLGA NPs encapsulating EVG and CUR (PLGA-EVG and PLGA-CUR) were prepared via the nanoprecipitation method. The NPs were characterized for size, zeta potential, and encapsulation efficiency (EE). Their therapeutic efficacy was evaluated in vitro using U1 macrophages and in vivo in Balb/c mice. Key parameters, including cytokine levels, oxidative stress markers, and neuronal marker expression, were analyzed. Results: The PLGA-EVG and PLGA-CUR NPs demonstrated high EE% (~90.63 ± 4.21 for EVG and 87.59 ± 3.42 for CUR) and sizes under 140 nm, ensuring blood-brain barrier (BBB) permeability. In vitro studies showed enhanced intracellular EVG concentrations and reductions in proinflammatory cytokines (IL-1β, TNFα, and IL-18) and improved antioxidant capacity in U1 macrophages. In vivo, the co-administration of NPs improved CNS drug delivery, reduced neuroinflammation and oxidative stress, and preserved neuronal markers (L1CAM, synaptophysin, NeuN, GFAP). Conclusions: PLGA-based co-delivery of EVG and CUR enhances ART CNS drug delivery, mitigating neuroinflammation and reducing oxidative stress. These findings highlight the potential of nanoparticle-based ART strategies to address limitations in current regimens and pave the way for more effective HAND therapies. Future studies should focus on optimizing formulations and evaluating safety in chronic HIV settings.

Early brain injury caused by subarachnoid hemorrhage (SAH) is associated with inflammatory response and ferroptosis. Curcumin alleviates neuroinflammation and oxidative stress by as yet unknown neuroprotective mechanisms. The objective of this study was to investigate the impact of curcumin on neuronal ferroptosis and microglia-induced neuroinflammation following SAH. By examining Nrf2/HO-1 expression levels and ferroptosis biomarkers expression both in vitro and in vivo, it was demonstrated that curcumin effectively suppressed ferroptosis in neurons after SAH through modulation of the Nrf2/HO-1 signaling pathway. Furthermore, by analyzing the expression levels of Nrf2, HO-1, p-p65, and inflammation-related genes, it was confirmed that curcumin could prevent the upregulation of pro-inflammatory factors following SAH by regulating the Nrf2/HO-1/NF-κB signaling pathway in microglia. The ability of curcumin to reduce neuronal damage and cerebral edemas after SAH in mice was validated using TUNEL staining, Nissl staining, and measurement of brain tissue water content. Additionally, through implementation of the modified Garcia test, open field test, and Y-maze test, it was established that curcumin ameliorated neurobehavioral impairments in mice post-SAH. Taken together, these data suggest that curcumin may offer a promising therapeutic approach for improving outcomes following SAH by concurrently attenuating neuronal ferroptosis and reducing neuroinflammation.

Curcumin has a wide range of application prospects, with various bioactivities in the food industry and in the biomedical field. However, curcumin has poor water solubility and is sensitive to pH, light and temperature. In this study, curcumin-chitooligosaccharide (CUR-COS) complexes were prepared via mechanochemical methods, and the CUR-COS complex was more soluble after freeze-drying (up to 862-fold greater than that of curcumin). The complex was characterized by SEM, XRD, FT-IR and thermal analysis, and its stability against pH, light and thermal treatment was evaluated. COSs could serve as carriers for curcumin delivery. Additionally, the antibacterial activity of the formed complex was determined. As a result, CUR-COS exhibited significantly better water solubility, enhanced stability, and stronger antibacterial properties than did pure CUR, offering a promising pathway for the extensive application of lipophilic natural products in foods, especially water-based products.

Diabetes mellitus (DM) is a long-term metabolic disease characterised by a controlled metabolism of fat, carbohydrates, and proteins. In recent decades, it has grown into a significant global public health issue. According to the International Diabetes Federation, there were 425 million DM globally in 2017, and the number might be increased to 629 million by 2045 (a global 48% increase). Approximately 4.2 million deaths globally attributed to DM occur before the age of 60. The existing class of anti-diabetic medications is limited by side effects, which has led to the hunt for novel inhibitors that specifically target the α-amylase and α-glucosidase enzymes. Curcumin is a small-molecular-weight compound found in the roots of the Curcuma longa L (C. longa). plant, which has been used for culinary, medicinal, and other purposes throughout Asia for thousands of years. Curcumin has potent anti-inflammatory, anti-cancer, anti-angiogenic, antispasmodic, antibacterial, and anti-parasitic qualities. Even though the potential of curcumin to cure DM has been well investigated, its low solubility, rapid metabolism, and short plasma half-life have limited its application in DM. Therefore, the objectives of this review were to review the chemical composition of C. longa, the structure of curcumin, the degradation of curcumin, and the effects of curcumin derivatives on anti-diabetic properties against α-amylase and α-glucosidase enzymes. The results showed that C. longa contains carbohydrates, moisture, protein, fat, minerals, volatiles, fibre, and curcuminoids. Among the curcuminoids, curcumin is 60-70% present in C. longa. Moreover, curcumin and its derivatives have a lot of potential for treating DM, which was highlighted in this review. This review emphasises the several biological applications of curcumin, which collectively establish the foundation for its anti-diabetic characteristics. Considering these results, curcumin derivatives may be considered as potential agents in the pharmacotherapeutic management of patients with DM.

Curcumin serves as a photosensitizer (PS) in the context of microbial inactivation when subjected to light exposure, to produce reactive oxygen species, which exhibit efficacy in eradicating microorganisms. This remarkable property underscores the growing potential of antimicrobial photodynamic therapy (aPDT) in the ongoing fight against bacterial infections. Considering this, we investigate the efficacy of various in vitro curcumin formulations within a PDT protocol designed to target Staphylococcus aureus. Specifically, we conduct a comparative analysis involving synthetic curcumin (Cur-Syn) and curcumin derivatives modified with chlorine (Cl), selenium (Se), and iodine (I) (Cur-Cl, Cur-Se, Cur-I). To assess the impact of aPDT, we subject S. aureus to incubation with curcumin, followed by irradiation at 450 nm with energy doses of 3.75, 7.5, and 15 J/cm2. Our investigation encompasses an evaluation of PS uptake and photobleaching across the various curcumin variants. Notably, all three modifications (Cur-Cl, Cur-Se, Cur-I) induce a significant reduction in bacterial viability, approximately achieving a 3-log reduction. Interestingly, the uptake kinetics of Cur-Syn and Cur-Se exhibit similarities, reaching saturation after 20 min. Our findings suggest that modifications to curcumin have a discernible impact on the photodynamic properties of the PS molecule.

This study aimed to use a new protein complex of Pennisetin (Pen) a non gluten protein of pearl millet and casein (Cas), for curcumin (Cur) extract encapsulation using simple or complex coacervation. The potential improvement of Cur antioxidant activities and α-amylase inhibition after encapsulation was explored. Complex microparticles of Pen and Cas with various ratios exhibited average diameters ranging from 1.95 ± 0.32 to 4.66 ± 0.99 μm, whereas the Cur loaded microparticles had average diameters ranging from 2.50 ± 0.89 to 5.27 ± 1.17 μm. FTIR analysis of Cur loaded microparticles showed the presence of specific peaks at 3757, 1754, 1157 and 856 cm-1 related to characteristic functional groups of Cur. This confirms the successful encapsulation of Cur. The major forces involved in microparticles formation were hydrophobic interaction and hydrogen bonding. The best encapsulation efficiency 68 % and loading capacity 17 % were obtained for the complex microparticles Pen:Cas (ratio 1:1.5). Encapsulating Cur within microparticles of Pen, Cas or their complexes significantly (p˂0.05) enhances their DPPH and ABTS.+ antioxidant activities and their pancreatic α-amylase inhibition percentage. These findings shed light on the potential use of Pen a non gluten protein, in its native form or complexed with Cas, as wall material for hydrophobic or hydrophilic bioactive compounds encapsulation.

Osteoarthritis is a degenerative joint disease that affects the aging population worldwide. It has an underlying inflammatory cause that leads to loss of chondrocytes, reducing the cartilage layer at the affected joints. Compounds with anti-inflammatory properties are potential therapeutic agents for osteoarthritis. Curcumin, derived from species of the Curcuma, is an anti-inflammatory compound. The purpose of this review is to summarize the anti-osteoarthritic effects of curcumin from clinical and preclinical studies. Many clinical trials have been conducted to determine curcumin's effectiveness in osteoarthritis patients. Available studies have shown that curcumin prevents chondrocyte apoptosis and inhibits the release of proteoglycans and metalloproteinases as well as the expression of cyclooxygenase, prostaglandin E-2, and inflammatory cytokines in chondrocytes. The mechanism of action of curcumin also involves multiple cell signaling pathways, including Nuclear factor kappa-B(NF-κB), Mitogen-activated protein kinase (MAPK), Wnt/β-catenin pathway (Wnt/β-catenin), The Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3), Nuclear factor erythroid 2-related factor 2/antioxidant response elements/heme oxygenase-1(Nrf2/ARE/HO-1), and Phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathways. Curcumin further reduced the release of inflammatory factors and apoptosis by inhibiting the activation of NF-κB. In addition, curcumin modulates the MAPK, Nrf2/ARE/HO-1, and PI3K/Akt/mTOR signaling pathways and affects cell proliferation and apoptosis processes, a series of effects that together promote the healthy state of chondrocytes. In conclusion, curcumin, as a natural plant compound, exhibits significant anti-inflammatory potential by modulating inflammatory factors associated with articular osteoarthritis through multiple mechanisms. Its protective effects on articular cartilage and synovium make it a promising candidate for the treatment of OA. Future studies should further explore the mechanism of action of curcumin and its optimal dosage and therapeutic regimen in clinical applications, to provide more effective therapeutic options for osteoarthritis patients.

A large body of evidence has shown that modulation of the nuclear receptors peroxisome proliferator-activated receptors (PPARs), the liver X receptors (LXRs), the proprotein convertase subtilisin/kexin type 9 (PCSK9) and inflammatory processes by natural compounds has hypolipidemic and anti-atherosclerotic effects. These beneficial outcomes are certainly related to the crucial function of these targets in maintaining cholesterol homeostasis and regulating systemic inflammation. Currently, the therapeutic scenario for cardiovascular diseases (CVD) offers a plethora of widely validated and functional pharmacological treatments to improve the health status of patients. However, patients are increasingly sceptical of pharmacological treatments which are often associated with moderate to severe side effects. The aim of our review is to provide a collection of the most recent scientific evidence on the most common phytochemicals, used for centuries in the Mediterranean diet and traditional chinese medicine that act on these key regulators of cholesterol homeostasis and systemic inflammation, which could constitute important tools for CVD management.

Peritoneal dialysis (PD) is considered a life-saving treatment for end-stage renal disease. However, prolonged PD use can lead to the development of peritoneal fibrosis (PF), diminishing its efficacy. Peritoneal mesothelial cells (PMCs) are key initiators of PF when they become damaged. Exposure to high glucose‑based peritoneal dialysis fluids (PDFs) contributes to PF development by directly affecting highly metabolically active PMCs. Recent research indicates that PMCs undergo metabolic reprogramming when exposed to high-glucose PDFs, including enhanced glycolysis, impaired oxidative phosphorylation, abnormal lipid metabolism, and mitochondrial dysfunction. Although this metabolic transition temporarily compensates for the cellular damage and maintains energy levels, its long-term impact on peritoneal tissue is concerning. Multiple studies have identified a close association between this shift in energy metabolism and PF, and may promote the progression of PF through various molecular mechanisms. This review explores recent findings regarding the role and mechanism of PMC metabolic reprogramming in PF progression. Moreover, it provides a summary of potential therapeutic strategies aimed at various metabolic processes, including glucose metabolism, lipid metabolism, and mitochondrial function. The review establishes that targeting metabolic reprogramming in PMCs may be a novel strategy for preventing and treating PD-associated fibrosis.

The alarming rise in bacterial infections including those caused by multidrug-resistant pathogens has garnered the attention of the scientific community, compelling them to explore as novel and effective alternatives to combat these infections. Moreover, the emerging viruses such as Influenza A virus subtype H1N1 (A/H1N1), Middle East Respiratory Syndrome Coronavirus (MERS-CoV), Ebolavirus, recent coronavirus (SARS-CoV-2), etc. also has a significant impact all over the world. Therefore, the management of all such infections without any side effects is one of the most important challenges for the scientific community. Hence, the development of novel and effective antimicrobial agents is a need of the hour. In this context, Curcuma longa, commonly known as turmeric, has been used as traditional medicine for centuries to manage and treat such infections. Its bioactive constituent, curcumin has garnered significant attention in medicine due to its multifunctional bioactivities. Apart from antimicrobial properties, it also possesses potent antioxidant and anti-inflammatory activities. However, available reports suggest that its low solubility, stability, and biocompatibility limit its use. Moreover, on the other hand, it has been reported that these limitations associated with the use of curcumin can be resolved by transforming it into its nano-form, specifically curcumin nanoparticles. Recent advancements have brought curcumin nanoparticles into the spotlight, showcasing superior properties and a broad spectrum of antimicrobial applications. In this review, we have mainly focused on antimicrobial potential of curcumin and nanocurcumin, mechanisms underpinning their antimicrobial actions. Moreover, other aspects of toxicity and safety guidelines for nano-based products have been also discussed.

The epithelial-to-mesenchymal transition (EMT) is a crucial step in metastasis formation. It enhances the ability of cancer cells' to self-renew and initiate tumors, while also increasing resistance to apoptosis and chemotherapy. Among the signaling pathways a few signaling pathways such as Notch, TGF-beta, and Wnt-beta catenin are critically involved in the epithelial-to-mesenchymal transition (EMT) acquisition. Therefore, regulating EMT is a key strategy for controlling malignant cell behavior. This is done by interconnecting other signaling pathways in many cancer types. Although there is extensive preclinical evidence regarding EMT's function in the development of cancer, there is still a deficiency in clinical translation at the therapeutic level. Thus, there is a need for medications that are both highly effective and with low cytotoxic for modulating EMT transitions at ground level. Thus, this led to the study of the evaluation and efficiency of phytochemicals found in dietary sources of fruits and vegetables and also the combination of small molecular repurposed drugs that can enhance the effectiveness of traditional cancer treatments. This review summarises major EMT-associated pathways and their cross talks with their mechanistic insights and the role of different dietary phytochemicals (curcumin, ginger, fennel, black pepper, and clove) and their natural analogs and also repurposed drugs (metformin, statin, chloroquine, and vitamin D) which are commonly used in regulating EMT in various preclinical studies. This review also investigates the concept of low-toxicity and broad spectrum ("The Halifax Project") approach which can help for site targeting of several key pathways and their mechanism. We also discuss the mechanisms of action, models for our dietary phytochemicals, and repurposed drugs and their combinations used to identify potential anti-EMT activities. Additionally, we also analyzed existing literature and proposed new directions for accelerating the discovery of novel drug candidates that are safe to administer.

Neurodegenerative diseases comprise a group of chronic, usually age-related, disorders characterized by progressive neuronal loss, deformation of neuronal structure, or loss of neuronal function, leading to a substantially reduced quality of life. They remain a significant focus of scientific and clinical interest due to their increasing medical and social importance. Most neurodegenerative diseases present intracellular protein aggregation or their extracellular deposition (plaques), such as α-synuclein in Parkinson's disease and amyloid beta (Aβ)/tau aggregates in Alzheimer's. Conventional treatments for neurodegenerative conditions incur high costs and are related to the development of several adverse effects. In addition, many patients are irresponsive to them. For these reasons, there is a growing tendency to find new therapeutic approaches to help patients. This review intends to investigate some phytocompounds' effects on neurodegenerative diseases. These conditions are generally related to increased oxidative stress and inflammation, so phytocompounds can help prevent or treat neurodegenerative diseases. To achieve our aim to provide a critical assessment of the current literature about phytochemicals targeting neurodegeneration, we reviewed reputable databases, including PubMed, EMBASE, and COCHRANE, seeking clinical trials that utilized phytochemicals against neurodegenerative conditions. A few clinical trials investigated the effects of phytocompounds in humans, and after screening, 13 clinical trials were ultimately included following PRISMA guidelines. These compounds include polyphenols (flavonoids such as luteolin and quercetin, phenolic acids such as rosmarinic acid, ferulic acid, and caffeic acid, and other polyphenols like resveratrol), alkaloids (such as berberine, huperzine A, and caffeine), and terpenoids (such as ginkgolides and limonene). The gathered evidence underscores that quercetin, caffeine, ginkgolides, and other phytochemicals are primarily anti-inflammatory, antioxidant, and neuroprotective, counteracting neuroinflammation, neuronal oxidation, and synaptic dysfunctions, which are crucial aspects of neurodegenerative disease intervention in various included conditions, such as Alzheimer's and other dementias, depression, and neuropsychiatric disorders. In summary, they show that the use of these compounds is related to significant improvements in cognition, memory, disinhibition, irritability/lability, aberrant behavior, hallucinations, and mood disorders.

The goal of this study was to evaluate the effect of the supplemental plant-based blend Phyto AquaNity (PAN) on growth, profitability and health status of Nile tilapia (O. niloticus) cultured in hapas. Juvenile fish of average weight 73 g were stocked in 2-m3 hapas in triplicates at a density of 20 fish m-3 (40 fish hapa-1). Four extruded diets were formulated following isonitrogenous (30% CP), isoenergetic (17 MJ kg-1) standards, with incorporation levels of 0, 0.25, 0.50, or 1.00 g of PAN kg-1 diet. Fish were fed the experimental diets at a daily rate of 2-3% of their body weight (BW) over 80 days. From this study, results showed that growth performance and tissue composition were not significantly impacted by these treatments. Feed intake exhibited a significant reduction while feed efficiency was improved in the groups fed 0.5 g kg-1. Diets supplemented with PAN were also more profitable than the control diet, with 0.5 g kg-1 indicating the highest return (9.24% increase). Digestive enzyme activity and hepatic enzyme activity were significantly improved with an increase in the level of PAN up to 0.50 g kg-1. In addition, immune parameters (lysozyme activity, alternative complement and phagocytic cells) and antioxidant enzymes (superoxide dismutase, glutathione peroxidase and catalase) were significantly enhanced with increasing PAN level up to 0.5 g kg-1 (p < 0.05). Gene expression of cytokines was also upregulated in fish fed with PAN at levels of up to 0.5 g kg-1 (p < 0.05). Moreover, the results showed that higher levels of PAN promoted the growth of beneficial bacteria while reducing the load of pathogenic bacteria. Additionally, intestinal fold length and goblet cell count were significantly increased in the group fed PAN up to 0.5 g kg-1. A quadratic regression analyses performed on feed efficiency, profitability, hepatic enzyme activity and gut microbial load revealed that 0.60-0.65 g kg-1 of feed were the optimal dosages. Regarding immunological and antioxidant responses, the optimal dosages ranged between 0.75 and 0.85 g kg-1. Overall, about 0.60-0.85 g PAN kg-1 feed is suggested for optimum performance, profitability, gut health and overall health status of Nile tilapia, depending on the target objective for which this product is added.

In this study, we investigated a new, simple, sensitive, selective and precise high-performance thin-layer chromatography (HPTLC) fingerprint and quantitative estimation method for the routine analysis of curcumin in Curcuma species viz. Curcuma amada, Curcuma caesia, Curcuma longa and Curcuma zedoaria. Linear ascending development was carried out in a twin-trough glass chamber saturated with toluene:acetic acid (4:1; v/v with 20 minutes of saturation). The plate was dried and analyzed by CAMAG TLC scanner III at white light and 366 nm. The system was found to give compact spots for curcumin (Rf 0.42). The relationship between the concentration of standard solutions and the peak response is linear within the concentration range of 10-70 ng/spot for curcumin. In result, curcumin was not detected in any of C. caesia extracts. The percentage of curcumin was found between 0.042 and 4.908 (%w/w) in different Curcuma species obtained by two different extraction methods viz. Soxhlet and sonication, respectively. Further, extraction via Soxhlet method is most suitable method to get higher curcumin content from rhizomes. The proposed HPTLC method may be use for routine quality testing and quantification of curcumin in Curcuma samples.

Lipid metabolism plays a crucial role in maintaining homeostasis and overall health, as lipids are essential molecules involved in bioenergetic processes. An increasing body of research indicates that disorders of lipid metabolism can contribute to the development and progression of various diseases, including hyperlipidemia, obesity, non-alcoholic fatty liver disease (NAFLD), diabetes mellitus, atherosclerosis, and cancer, potentially leading to poor prognoses. The activation of the oxidative stress pathway disrupts lipid metabolism and induces cellular stress, significantly contributing to metabolic disorders. A well-documented crosstalk and interconnection between these metabolic disorders exists. Consequently, researchers have sought to identify antioxidant-rich substances in readily accessible everyday foods for potential use as complementary therapies. Curcumin, known for its anti-inflammatory and antioxidant properties, has been shown to enhance cellular antioxidant activity, mitigate oxidative stress, and alleviate lipid metabolism disorders by reducing reactive oxygen species (ROS) accumulation. These effects include decreasing fat deposition, increasing fatty acid uptake, and improving insulin sensitivity. A review of the existing literature reveals numerous studies emphasizing the role of curcumin in the prevention and management of metabolic diseases. Curcumin influences metabolic disorders through multiple mechanisms of action, with the oxidative stress pathway playing a central role in various lipid metabolism disorders. Thus, we aimed to elucidate the role of curcumin in various metabolic disorders through a unified mechanism of action, offering new insights into the prevention and treatment of metabolic diseases. Firstly, this article provides a brief overview of the basic pathophysiological processes of oxidative stress and lipid metabolism, as well as the role of oxidative stress in the pathogenesis of lipid metabolism disorders. Notably, the article reviews the role of curcumin in mitigating oxidative stress and in preventing and treating diseases associated with lipid metabolism disorders, including hyperlipidemia, non-alcoholic fatty liver disease (NAFLD), atherosclerosis, obesity, and diabetes, thereby highlighting the therapeutic potential of curcumin in lipid metabolism-related diseases.

Gastric ulcer is a common disorder of the digestive system. The combination of turmeric and honey is known to treat stomach ulcers. However, curcumin, an active component in turmeric, has limitations, i.e., poor water solubility and low oral bioavailability. Therefore, turmeric and honey were formulated into a nanoemulsion with black pepper to enhance curcumin bioavailability. The study followed a systematic approach to optimize the nanoemulsion formula, determine stability, and evaluate ulcer healing activity in rats with ethanol-induced gastric ulcers. Nanoemulsion was prepared using a low-energy emulsification method called emulsion phase inversion (EPI). Two stability evaluations were carried out, i.e., storage and freeze-thaw stability tests. The organoleptic, droplet size, polydispersity index, pH, viscosity, and curcumin content of the nanoemulsion were evaluated. Male Wistar albino rats were induced with 96% ethanol for six days. The rats were divided into six groups, i.e., healthy control, ulcerated control, omeprazole, two different doses of turmeric, honey, and black pepper nanoemulsion (NTBH1 and NTBH2), and turmeric and honey nanoemulsion (NTH). The antiulcer activity was determined by measuring the ulcer area, ulcer index, curative index, ulcer severity score, and histology. The best formula with the smallest droplet size, i.e., 144.6±3.8 nm, was obtained from the nanoemulsion using Tween 80 as surfactant, glycerin as cosolvent, and sodium alginate as viscosity enhancer. The result showed that the nanoemulsion was stable after being stored at 25 and 40°C for four weeks and after six cycles of freeze-thaw test. The ulcer index of the ulcerated rats from the lowest to the highest, i.e., NTBH2, omeprazole, NTH, and NTBH1. In conclusion, the nanoemulsion developed in this study containing turmeric, honey, and black pepper holds promising potential in treating gastric ulcers, offering a hopeful outlook for future treatments.