Depression is a prevalent psychiatric disorder and one of the leading causes of disability worldwide. Previous studies have shown that Semen Cuscutae flavonoids (SCFs) exert antidepressant effects by modulating the microbiota-neuroinflammation axis and ameliorating hippocampal metabolic disturbances. However, the impact of SCFs on gut microbiota and related metabolomics remains largely undefined. Given that the gut microbiota has been proven to play a significant role in the etiology of depression and serves as a promising target for its treatment in humans, this study aims to elucidate the antidepressant effects of SCFs and to investigate how they modulate microbial and metabolic pathways to alleviate depressive symptoms.

Chronic unpredictable mild stress (CUMS)-induced mice were used as a depression model. The normal mice and CUMS-induced mice were treated with either vehicle or with SCFs. A range of standardized behavioral assays and physiological indicators were employed to evaluate the antidepressant effects of SCFs. Upon the confirmation of the effectiveness of the SCFs treatment, the composition, richness, and diversity of the fecal microbiota were assessed using 16S rRNA gene sequencing. Additionally, fecal metabolic profiling was analyzed using UHPLC-MS/MS-based metabolomics. Multivariate data analysis was subsequently performed to identify differential metabolites and characterize alterations in fecal metabolites. Furthermore, a correlation analysis between differential metabolites and key microbiota was conducted.

SCFs significantly ameliorated depressive behaviors and the dysregulated diversity of fecal microbiota induced by CUMS. SCFs enhanced the gut microbiota structure in the CUMS group by increasing the Firmicutes/Bacteroidota ratio, significantly elevating the abundance of Firmicutes, Lactobacillus, Limosilactobacillus, and Actinobacteria while reducing the abundance of Bacteroidota and Bacteroides in CUMS-treated mice. Fecal metabolomics analyses revealed that SCFs could modulate metabolic pathways, including aldosterone synthesis and secretion, arachidonic acid metabolism, and primary bile acid biosynthesis.

Mice with depression induced by CUMS exhibited disturbances in both their gut microbiota and fecal metabolism. However, SCFs restored the balance of the microbial community and corrected metabolic disturbances in feces, exerting antidepressant effects through a multifaceted mechanism.

Nonalcoholic steatohepatitis (NASH) is a significant threat to human health. Our previous study revealed that salidroside attenuated NASH and regulated the gut microbiota. However, whether the therapeutic effect of salidroside depends on gut microbiota remains to be determined. Therefore, we conducted further experiments to elucidate the essential functions of gut microbiota-associated metabolic pathways in the anti-NASH effects of salidroside. Our results showed that salidroside effectively alleviated lipid accumulation and inflammatory injury in NASH mice. 16S rRNA sequencing revealed that salidroside increased the abundance of Bacteroides. Mice receiving fecal microbiota transplantation (FMT) from salidroside-treated also presented less hepatic steatosis and higher abundance of Bacteroides. Antibiotics eliminated the effects of salidroside on hepatic steatosis and the gut microbiota. Mechanistically, salidroside and FMT from salidroside-treated altered the bile acid (BA) profile by decreasing the levels of conjugated BAs and tauro-α/β-muricholic acid and activated downstream farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5). Furthermore, we found that inhibitors of bile salt hydrolase (BSH) and FXR/TGR5 abolished the effects of salidroside and reduced downstream carnitine palmitoyltransferase 1α and lipoprotein lipase expression. These data demonstrate that salidroside attenuated NASH via gut microbiota-BA-FXR/TGR5 signaling pathway and reveal the underlying mechanism of salidroside on NASH.

The global incidence of liver diseases is on the rise, and targeting gut microbiota has become a new strategy for treating liver diseases. This study provides a comprehensive and objective analysis of the potential protective role of gut microbiota in liver disease, highlighting the need for continued research in this area.

After literature screening, 24 related articles were included in the study. After article quality and risk of bias assessment, data extraction and data collation were carried out, and then comprehensive analysis was carried out using stata12.0 software.

From the perspective of microbial community, most of the microbial communities at the phylum level are risk factors; from the perspective of the top ten families, the intestinal microbial communities play an obvious harmful role in Primary Biliary Cholangitis.From the perspective of disease, the microbial communities at the genus level mostly have protective effects on Chronic Hepatitis B ,Fatty Liver;and Primary Liver Cancer.

Gut microbiota plays a significant role in the occurrence of liver diseases, and different bacterial levels play different roles in the disease.

Addictive substance use disorder has a wide range of effects on the intestinal barrier, including damage to the biological, chemical, mechanical, and immune barriers. Damage to the intestinal barrier caused by addictive substance use disorder allows harmful substances and bacteria to cross the intestinal barrier into the circulatory system, leading to systemic inflammatory responses and immune imbalances. In addition, the interaction between the gut flora and the central nervous system is recognized as an important component of the gut-brain axis. Gut barrier damage leads to dysbiosis, which in turn affects brain function by activating immune cells and releasing inflammatory factors. This may lead to altered mood and cognitive function, increased addictive substance cravings, and dependence. Recent research has indicated that reshaping the gut-brain axis and adjusting the composition and abundance of gut microbiota holds promise in alleviating withdrawal symptoms with addictive substance dependence. This article reviews the effects of addictive substance use disorder on the intestinal barrier and explores the possibility of improving addictive substance dependence by treating gut barrier damage.

Acute-on-chronic liver failure (ACLF) is a severe condition in patients with decompensated liver cirrhosis, marked by high short-term mortality. Recent experimental and clinical evidence has linked intestinal dysfunction to both the initiation of ACLF as well as disease outcome. This review discusses the significant role of the gut-liver axis in ACLF pathogenesis, highlighting recent advances. Gut mucosal barrier disruption, gut dysbiosis, and bacterial translocation emerge as key factors contributing to systemic inflammation in ACLF. Different approaches of therapeutically targeting the gut-liver axis via farnesoid X receptor agonists, nonselective beta receptor blockers, antibiotics, and probiotics are discussed as potential strategies mitigating ACLF progression. The importance of understanding the distinct pathophysiology of ACLF compared with other stages of liver cirrhosis is highlighted. In conclusion, research findings suggest that disruption of intestinal integrity may be an integral component of ACLF pathogenesis, paving the way for novel diagnostic and therapeutic approaches to manage this syndrome more effectively.

Cholangiocarcinoma (CCA) is a rare but highly malignant carcinoma of bile duct epithelial cells with a poor prognosis. The major risk factors of CCA carcinogenesis and progression are cholestatic liver diseases. The key feature of primary sclerosing cholangitis and primary biliary cholangitis is chronic cholestasis. It indicates a slowdown of hepatocyte secretion of biliary lipids and metabolites into bile as well as a slowdown of enterohepatic circulation (bile acid recirculation) of bile acids with dysbiosis of the gut microbiome. This leads to enterohepatic recirculation and an increase of toxic secondary bile acids. Alterations of serum and liver bile acid compositions via the disturbed enterohepatic circulation of bile acids and the disturbance of the gut microbiome then activate a series of hepatic and cancer cell signaling pathways that promote CCA carcinogenesis and progression. This review focuses on the mechanistic roles of bile acids and the gut microbiome in the pathogenesis and progression of CCA. It also evaluates the therapeutic potential of targeting the gut microbiome and bile acid-mediated signaling pathways for the therapy and prophylaxis of CCA.

Over the past half a century the Western diet (WD) has become saturated with food additives. During the same time, there has been an increase in Western diseases, such as inflammatory bowel disease (IBD) and metabolic syndrome (MetS). Emerging research has shown that food additives may be implicated in these diseases. However, critics have suggested that some of this research is problematic and may cause unnecessary fear amongst consumers. Here we review the emerging research concerning food additives and their implication in IBD and MetS, and criticisms thereof. To make the review more relevant to the WD, we only included common food additives, selected using supermarket data. Over a dozen common food additives from four categories were identified for their potential role in directly promoting these diseases. A consistent limitation of the research was the use of unrealistic human exposure conditions, such as high doses and modes of administration, as well as a lack of human trials. Another limitation was the absence of studies investigating the potential synergetic effect of consuming multiple food additives, as is common in the WD. Despite the limitations, there is some evidence that common food additives may be contributing to these additives, especially via their dysbiotic effect on the gut microbiota.

Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a chronic liver disease. The development of MASLD is influenced by a multitude of diseases associated with modern lifestyles, including but not limited to diabetes mellitus, hypertension, hyperlipidaemia and obesity. These conditions are often consequences of the adoption of unhealthy habits, namely a sedentary lifestyle, a lack of physical activity, poor dietary choices and excessive alcohol consumption. The treatment of MASLD is primarily based on modifying the patient's lifestyle and pharmacological intervention. Despite the absence of FDA-approved pharmacological agents for the treatment of MASLD, several potential therapeutic modalities have demonstrated efficacy in reversing the histopathological features of the disease. Among the botanical ingredients belonging to the flavonoid group is quercetin (QE). QE has been demonstrated to possess a number of beneficial physiological effects, including anti-inflammatory, anticancer and antifungal properties. Additionally, it functions as a natural antioxidant. Preclinical evidence indicates that QE may play a beneficial role in reducing liver damage and improving metabolic health. Early human studies also suggest that QE may be an effective treatment for MASLD due to its antioxidant, anti-inflammatory, and lipid-regulating properties. This review aims to summarize the available information on the therapeutic effects of QE in MASLD.

With the rising prevalence of chronic liver diseases worldwide, there exists a need to diversify our artillery to incorporate a plethora of diagnostic and therapeutic methods to combat this disease. Currently, the most common causes of liver disease are non-alcoholic fatty liver disease, hepatitis, and alcoholic liver disease. Some of these chronic diseases have the potential to transform into hepatocellular carcinoma with advancing fibrosis. In this review, we analyse the relationship between the gut and liver and their significance in liver disease. This two-way relationship has interesting effects on each other in liver diseases. The gut microbiota, through its metabolites, influences the metabolism in numerous ways. Careful manipulation of its composition can lead to the discovery of numerous therapeutic potentials that can be applied in the treatment of various liver diseases. Numerous cohort studies with a pan-omics approach are required to understand the association between the gut microbiome and hepatic disease progression through which we can identify effective ways to deal with this issue.

Diabetic nephropathy (DN) is a prevalent microvascular complication that occurs often in individuals with diabetes. It significantly raises the mortality rate of affected patients. Therefore, there is an urgent need to identify therapeutic targets for controlling and preventing the occurrence and development of DN. Bile acids (BAs) are now recognized as intricate metabolic integrators and signaling molecules. The activation of BAs has great promise as a therapeutic approach for preventing DN, renal damage caused by obesity, and nephrosclerosis. The nuclear receptors (NRs), farnesoid X receptor (FXR), pregnane X receptor (PXR), vitamin D receptor (VDR); and the G protein-coupled BA receptor, Takeda G-protein-coupled receptor 5 (TGR5) have important functions in controlling lipid, glucose, and energy metabolism, inflammation, as well as drug metabolism and detoxification. Over the past 10 years, there has been advancement in comprehending the biology and processes of BA receptors in the kidney, as well as in the creation of targeted BA receptor agonists. In this review, we discuss the role of BA receptors, FXR, PXR, VDR, and TGR5 in DN and their role in renal physiology, as well as the development and application of agonists that activate BA receptors for the treatment of kidney diseases.

The gut microbiota is believed to be directly involved in the etiology and development of chronic liver diseases. However, the holistic characterization of the gut bacteriome, mycobiome, and virome in patients with chronic hepatitis B-related liver fibrosis (CHB-LF) remains unclear.

In this study, we analyzed the multi-kingdom gut microbiome (i.e., bacteriome, mycobiome, and virome) of 25 CHB-LF patients and 28 healthy individuals through whole-metagenome shotgun sequencing of their stool samples.

We found that the gut bacteriome, mycobiome, and virome of CHB-LF patients were fundamentally altered, characterized by a panel of 110 differentially abundant bacterial species, 16 differential fungal species, and 90 differential viruses. The representative CHB-LF-enriched bacteria included members of Blautia_A (e.g., B. wexlerae, B. massiliensis, and B. obeum), Dorea (e.g., D. longicatena and D. formicigenerans), Streptococcus, Erysipelatoclostridium, while some species of Bacteroides (e.g., B. finegoldii and B. thetaiotaomicron), Faecalibacterium (mainly F. prausnitzii), and Bacteroides_A (e.g., B. plebeius_A and B. coprophilus) were depleted in patients. Fungi such as Malassezia spp. (e.g., M. japonica and M. sympodialis), Candida spp. (e.g., C. parapsilosis), and Mucor circinelloides were more abundant in CHB-LF patients, while Mucor irregularis, Phialophora verrucosa, Hortaea werneckii, and Aspergillus fumigatus were decreases. The CHB-LF-enriched viruses contained 18 Siphoviridae, 12 Myoviridae, and 1 Podoviridae viruses, while the control-enriched viruses included 16 Siphoviridae, 9 Myoviridae, 2 Quimbyviridae, and 1 Podoviridae_crAss-like members. Moreover, we revealed that the CHB-LF-associated gut multi-kingdom signatures were tightly interconnected, suggesting that they may act together on the disease. Finally, we showed that the microbial signatures were effective in discriminating the patients from healthy controls, suggesting the potential of gut microbiota in the prediction of CHB-LF and related diseases.

In conclusion, our findings delineated the fecal bacteriome, mycobiome, and virome landscapes of the CHB-LF microbiota and provided biomarkers that will aid in future mechanistic and clinical intervention studies.

Bile acids are synthesised in the liver and are essential amphiphilic steroids for maintaining the balance of cholesterol and energy metabolism in livestock and poultry. They can be used as novel feed additives to promote fat utilisation in the diet and the absorption of fat-soluble substances in the feed to improve livestock performance and enhance carcass quality. With the development of understanding of intestinal health, the balance of bile acid metabolism is closely related to the composition and growth of livestock intestinal microbiota, inflammatory response, and metabolic diseases. This paper systematically reviews the effects of bile acid metabolism on gut health and gut microbiology in livestock. In addition, our paper summarised the role of bile acid metabolism in performance and disease control.

The impact of dietary nutrients on body growth performance and the composition of gut microbes and metabolites is well-established. In this study, we aimed to determine whether dietary protein can regulate the physiological indexes and changes the intestinal tissue morphology in rats, and if dietary protein was a crucial regulatory factor for the composition, function, and metabolic pathways of the gut microbiota.

A total of thirty male Sprague Dawley (SD) rats (inbred strain, weighted 110 ± 10 g) were randomly assigned to receive diets containing animal-based protein (whey protein, WP), plant-based protein (soybean protein, SP), or a blended protein (soybean-whey proteins, S-WP) for a duration of 8 weeks. To investigate the effects of various protein supplement sources on gut microbiota and metabolites, we performed a high throughput 16S rDNA sequencing association study and fecal metabolomics profiling on the SD rats. Additionally, we performed analyses of growth indexes, serum biochemical indexes, and intestinal morphology.

The rats in S-WP and WP group exhibited a significantly higher body weight and digestibility of dietary protein compared to the SP group (P < 0.05). The serum total protein content of rats in the WP and S-WP groups was significantly higher (P < 0.05) than that in SP group, and the SP group exhibited significantly lower (P < 0.05) serum blood glucose levels compared to the other two groups. The morphological data showed the rats in the S-WP group exhibited significantly longer villus height and shallower crypt depth (P < 0.05) than the SP group. The gut microbial diversity of the SP and S-WP groups exhibited a higher level than that of the WP group, and the microbiomes of the WP and S-WP groups are more similar compared to those of the SP group. The Arachidonic acid metabolism pathway is the most significant KEGG pathway when comparing the WP group and the SP group, as well as when comparing the SP group and the S-WP group.

The type of dietary proteins exerted a significant impact on the physiological indices of SD rats. Intake of S-WP diet can enhance energy provision, improve the body's digestion and absorption of nutrients, as well as promote intestinal tissue morphology. In addition, dietary protein plays a crucial role in modulating fecal metabolites by regulating the composition of the gut microbiota. Metabolomics analysis revealed that the changes in the levels of arachidonic acid metabolites and secondary bile acid metabolite induced by Clostridium_sensu_stricto_1 and [Eubacterium]_coprostanoligenes_group maybe the primarily causes of intestinal morphological differences.

The Farnesoid X receptor (FXR) is a key transcription factor that is involved in the bile acid signaling network. The modulation of the FXR activity influences glucose and lipid homeostasis, reduces obesity and insulin resistance, as well as it regulates the pathogenesis of inflammatory and metabolic disorders. FXR ligands have therefore emerged in drug discovery as promising therapeutic agents for the prevention and treatment of gastrointestinal and liver diseases, including cancer.

Recent advances in the field of FXR modulators are reviewed, with a particular attention on patent applications filed in the past 5 years related to both the discovery and development of FXR targeting drugs.

FXR agonists have proven their efficacy and safety in humans and have shown a significant potential as clinical agents to treat metabolic and inflammatory associated conditions. However, several challenges, including adverse events such as pruritus, remain to be solved. Current studies aim to gain insights into the pathophysiological mechanisms by which FXR regulates metabolism and inflammation in terms of tissue/organ/isoform-specificity, post-translational modifications and coregulatory proteins, on the route of novel, improved FXR modulators.

Chlorogenic acid (CGA) is a natural polyphenol found in coffee, tea, vegetables, and fruits. It exhibits strong antioxidant activity and possesses several other biological properties, including anti-inflammatory effects, antimicrobial activity, and insulin-sensitizing properties. Moreover, it may improve lipid and glucose metabolism. This review summarizes the available information on the therapeutic effect of CGA in metabolic dysfunction-associated steatotic liver disease (MASLD). As the literature search engine, the browsers in the PubMed, Scopus, Web of Science databases, and ClinicalTrials.gov register were used. Animal trials and clinical studies suggest that CGA has promising therapeutic potential in treating MASLD and hepatic steatosis. Its mechanisms of action include antioxidant, anti-inflammatory, and anti-apoptotic effects via the activation of the Nrf2 signaling pathway and the inhibition of the TLR4/NF-κB signaling cascade. Furthermore, the alleviation of liver disease by CGA also involves other important molecules such as AMPK and important physiological processes such as the intestinal barrier and gut microbiota. Nevertheless, the specific target cell and key molecule to which CGA is directed remain unidentified and require further study.

Chronic hypoxia, common in neonates, disrupts gut microbiota balance, which is crucial for brain development. This study utilized cyanotic congenital heart disease (CCHD) patients and a neonatal hypoxic rat model to explore the association. Both hypoxic rats and CCHD infants exhibited brain immaturity, white matter injury (WMI), brain inflammation, and motor/learning deficits. Through 16s rRNA sequencing and metabolomic analysis, a reduction in B. thetaiotaomicron and P. distasonis was identified, leading to cholic acid accumulation. This accumulation triggered M1 microglial activation and inflammation-induced WMI. Administration of these bacteria rescued cholic acid-induced WMI in hypoxic rats. These findings suggest that gut microbiota-derived cholic acid mediates neonatal WMI and brain inflammation, contributing to brain immaturity under chronic hypoxia. Therapeutic targeting of these bacteria provides a non-invasive intervention for chronic hypoxia patients.

The etiopathogenesis of diverticulitis, among the most common gastrointestinal diagnoses, remains largely unknown. By leveraging stool collected within a large prospective cohort, we performed shotgun metagenomic sequencing and untargeted metabolomics profiling among 121 women diagnosed with diverticulitis requiring antibiotics or hospitalizations (cases), matched to 121 women without diverticulitis (controls) according to age and race. Overall microbial community structure and metabolomic profiles differed in diverticulitis cases compared to controls, including enrichment of pro-inflammatory Ruminococcus gnavus, 1,7-dimethyluric acid, and histidine-related metabolites, and depletion of butyrate-producing bacteria and anti-inflammatory ceramides. Through integrated multi-omic analysis, we detected covarying microbial and metabolic features, such as Bilophila wadsworthia and bile acids, specific to diverticulitis. Additionally, we observed that microbial composition modulated the protective association between a prudent fiber-rich diet and diverticulitis. Our findings offer insights into the perturbations in inflammation-related microbial and metabolic signatures associated with diverticulitis, supporting the potential of microbial-based diagnostics and therapeutic targets.

The gut-liver axis has emerged as a focal point in chronic liver disorders, prompting more research into the role of the gut microbiota in liver cirrhosis. In individuals with liver cirrhosis, changes in the structure and function of the gut microbiota are closely tied to clinical prognosis. However, there is a scarcity of bibliometric evaluations conducted in this particular field.

This study is aiming to conduct a complete analysis of the knowledge structure and centers pertaining to gut microbiota in liver cirrhosis using bibliometric methods. Publications on gut microbiota and liver cirrhosis from 2001 to 2023 are sourced from the Web of Science Core Collection. For the bibliometric analysis, we employ VOSviewer, CiteSpace, and the R package "bibliometrix".

Our study encompasses a comprehensive collection of 3109 articles originating from 96 countries, with notable contributions from leading nations such as the United States and China. The quantity of publications concerning the gut microbiota of liver cirrhosis rises annually. The University of California San Diego, Virginia Commonwealth University, Zhejiang University are the primary research institutions. World Journal of Gastroenterology publishes the most papers in this field, while hepatology is the most frequently co-cited journal. These publications come from a total of 15,965 authors, and the most prolific authors are Bajaj Jasmohan S., Schnabl Bernd and Gillevet Patrick M., while the most co-cited authors are Bajaj Jasmohan S., Younossi Zobair M., and Reiner Wiest. In addition, "dysbiosis", "gut microbiota", "intestinal barrier", "fecal microbiota transplantation", and "complement-system" are the primary keywords of research trends in recent years.

This study offering a comprehensive insight into the research dynamics surrounding gut microbiota in patients with liver cirrhosis. It delineates the current research frontiers and hotspots, serving as a valuable guide for scholars.

Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific liver disease associated with a high incidence of complications in the mid and late stages of gestation. This study investigates differences in the composition of intestinal flora among pregnant women diagnosed with ICP, employing Illumina MiSeq high-throughput sequencing technology.

This case-control study obtained patient data from the hospital information system (HIS) and the laboratory information system (LIS). Fecal samples were collected from 25 pregnant women who did not undergo intestinal preparation before delivery between December 2020 and March 2021. Whole-genome analysis was performed. PCR was used to amplify the 16S rRNA V3-V4 variable region, which was then sequenced. Alpha and beta diversity were computed, and the maternal intestinal flora's abundance and composition characteristics were analyzed. Differences in intestinal flora between the two sample groups were examined.

Bacteroides and Proteobacteria exhibited positive correlations with TBIL and IBIL. Betaproteobacteria, Gammaproteobacteria, and Erysipeiotrichi showed positive correlations with TBIL, IBIL, and DBIL, while Lactobacillus, Delftia, and Odoribacter demonstrated positive correlations with ALT.

The ICP group displayed significantly higher levels of total bile acid and ALT compared to the control group. The intestinal flora composition comprised four primary phyla: Firmicutes, Actinobacteria, Bacteroidetes, and Proteobacteria. ICP patients exhibited a lower relative abundance of intestinal flora across different levels of community composition when compared to the control group. Specific correlations between certain intestinal flora and clinical liver parameters were identified.

Minimal hepatic encephalopathy (MHE) negatively affects the prognosis of cirrhosis, but treatment is not standard. Rifamycin SV MMX (RiVM) is a nonabsorbable rifampin derivative with colonic action.

In a phase 2 placebo-controlled, double-blind randomized clinical trial patients with MHE were randomized to RiVM or placebo for 30 days with a 7-day follow-up. The primary endpoint was a change in stool cirrhosis dysbiosis ratio. Gut-brain (cognition, stool/salivary microbiome, ammonia, brain magnetic resonance spectroscopy), inflammation (stool calprotectin/serum cytokines), patient-reported outcomes (sickness impact profile: total/physical/psychosocial, high = worse), and sarcopenia (handgrip, bioelectric impedance) were secondary. Between/within groups and delta (post-pre) comparisons were performed.

Thirty patients (15/group) were randomized and completed the study without safety concerns. While cirrhosis dysbiosis ratio was statistically similar on repeated measures ANOVA (95% CI: -0.70 to 3.5), ammonia significantly reduced (95% CI: 4.4-29.6) in RiVM with changes in stool microbial α/β-diversity. MHE status was unchanged but only serial dotting (which tests motor strength) improved in RiVM-assigned patients. Delta physical sickness impact profile (95% CI: 0.33 = 8.5), lean mass (95% CI: -3.3 to -0.9), and handgrip strength (95% CI: -8.1 to -1.0) improved in RiVM versus placebo. Stool short-chain fatty acids (propionate, acetate, and butyrate) increased post-RiVM. Serum, urine, and stool bile acid profile changed to nontoxic bile acids (higher hyocholate/ursodeoxycholate and lower deoxycholate/lithocholate) post-RiVM. Serum IL-1β and stool calprotectin decreased while brain magnetic resonance spectroscopy showed higher glutathione concentrations in RiVM.

RiVM is well tolerated in patients with MHE with changes in stool microbial composition and function, ammonia, inflammation, brain oxidative stress, and sarcopenia-related parameters without improvement in cognition. RiVM modulates the gut-brain axis and gut-muscle axis in cirrhosis.

The gastrointestinal bile acid (BA)/microbiota axis has emerged as a potential mediator of health and disease, particularly in relation to pathologies such as inflammatory bowel disease (IBD) and colorectal cancer. Whilst it presents an exciting new avenue for therapies, it has not yet been characterized in surgical resection of the ileum, where BA reabsorption occurs. The identification of BA/microbiota signatures may provide future therapies with perioperative personalized medicine. In this work we conduct a systematic review with the aim of investigating the microbiome and BA changes that are associated with resection of the ileum.

The databases included were MEDLINE, EMBASE, Web of Science and Cochrane libraries. The outcomes of interest were faecal microbiome and BA signatures after ileal resection.

Of the initial 3106 articles, three studies met the inclusion/exclusion criteria for data extraction. A total of 257 patients (46% surgery, 54% nonsurgery controls) were included in the three studies. Two studies included patients with short bowel syndrome and the other included patients with IBD. Large-scale microbiota changes were reported. In general, alpha diversity had decreased amongst patients with ileal surgery. Phylum-level changes included decreased Bacteroidetes and increased Proteobacteria and Fusobacteria in patients with an intestinal resection. Surgery was associated with increased total faecal BAs, cholic acid and chenodeoxycholic acid. There were decreases in deoxycholic acid and glycine and taurine conjugated bile salts. Integrated BA and microbiota data identified correlations with several bacterial families and BA.

The BA/microbiota axis is still a novel area with minimal observational data in surgery. Further mechanistic research is necessary to further explore this and identify its role in improving perioperative outcomes.

The Antiviral Granules (AG) are derived from the classical famous prescription, which is composed of 9 traditional Chinese medicines, namely Radix Isatidis (called Banlangen, BLG in Chinese), Forsythiae Fructus (called Lianqiao, LQ in Chinese), Gypsum fibrosum, Anemarrhenae Rhizoma (called Zhimu, ZM in Chinese), Phragmitis Rhizoma (called Lugen, LG in Chinese), Rehmanniae Radix (called Dihuang, DH in Chinese), Pogostemonis Herba (called Guanghuoxiang, GHX in Chinese), Acori Tatarinowii Rhizoma (called Shichangpu, SCP in Chinese), and Curcumae Radix (called Yujin, YJ in Chinese), and has shown an excellent therapeutic effect in clinical treatment of influenza. However, there are few studies on the anti-influenza mechanism of AG, and the mechanism of action is still unclear.

The purpose is to provide the latest information about the clinical efficacy, pharmacodynamic composition and mechanism of AG based on scientific literature, so as to enhance the utilization of AG in the treatment of influenza and related diseases, and promote the development and innovation of novel anti-influenza drugs targeting the influenza virus.

Enter the data retrieval room, search for Antiviral Granules, as well as the scientific names, common names, and Chinese names of each Chinese medicine. Additionally, search for the relevant clinical applications, pharmacodynamic composition, pharmacological action, and molecular mechanism of both Antiviral Granules and single-ingredient medicines. Keywords includes terms such as "antiviral granules", "influenza", "Isatis indigotica Fort.", "Radix Isatidis", "Banlangeng", "pharmacology", "clinical application", "pharmacologic action", etc. and their combinations. Obtain results from the Web of Science, PubMed, Google Scholar, Sci Finder Scholar, CNKI and other resources.

AG is effective in the treatment of influenza and is often used in combination with other drugs to treat viral diseases. Its chemical composition is complex, including alkaloids, polysaccharides, volatile oils, steroid saponins, phenylpropanoids, terpenoids and other compounds. These compounds have a variety of pharmacological activities, which can interfere with the replication cycle of the influenza virus, regulate RIG-I-MAVS, JAK/STAT, TLRs/MyD88, NF-κB signaling pathways and related cytokines, regulate intestinal microorganisms, and protect both the lungs and extrapulmonary organs.

AG can overcome the limitations of traditional antiviral drug therapy, play a synergistic role in fighting influenza virus with the characteristics of multi-component, multi-pathway and multi-target therapy, and reverse the bodily function damage caused by influenza virus. AG may be a potential drug in the prevention and treatment of influenza and related diseases.

Short-chain fatty acids (SCFAs), produced by the gut microbiota, are thought to exert an anti-inflammatory effect on the host immune system. The levels of SCFAs and abundance of the microbiota that produce them are depleted in multiple sclerosis (MS), an autoimmune disease of the central nervous system (CNS). The mechanisms leading to this depletion are unknown. Using experimental autoimmune encephalomyelitis (EAE) as a model for MS, we have previously shown that gut microbiomes divergent in their abundance of specific commensal Lactobacillaceae, Limosilactobacillus reuteri (L. reuteri) and Ligilactobacillus murinus (L. murinus), differentially impact CNS autoimmunity. To determine the underlying mechanisms, we employed colonization by L. reuteri and L. murinus in disparate gut microbiome configurations in vivo and in vitro, profiling their impact on gut microbiome composition and metabolism, coupled with modulation of dietary fiber in the EAE model.

We show that stable colonization by L. reuteri, but not L. murinus, exacerbates EAE, in conjunction with a significant remodeling of gut microbiome composition, depleting SCFA-producing microbiota, including Lachnospiraceae, Prevotellaceae, and Bifidobacterium, with a net decrease in bacterial metabolic pathways involved in butyrate production. In a minimal microbiome culture model in vitro, L. reuteri directly inhibited SCFA-producer growth and depleted butyrate. Genomic analysis of L. reuteri isolates revealed an enrichment in bacteriocins with known antimicrobial activity against SCFA-producing microbiota. Functionally, provision of excess dietary fiber, as the prebiotic substrate for SCFA production, elevated SCFA levels and abrogated the ability of L. reuteri to exacerbate EAE.

Our data highlight a potential mechanism for reduced SCFAs and their producers in MS through depletion by other members of the gut microbiome, demonstrating that interactions between microbiota can impact CNS autoimmunity in a diet-dependent manner. These data suggest that therapeutic restoration of SCFA levels in MS may require not only dietary intervention, but also modulation of the gut microbiome.

Background: Hepatic encephalopathy (HE) caused by cirrhosis has severe consequences on an individual's lifespan, leading to long-term liver complications and potentially life-threatening outcomes. Despite recent interest in this condition, the effectiveness of secondary prophylaxis involving rixafimin, lactulose, or L-ornithine L-aspartate (LOLA) may be hindered by the unique microbial profiles each patient possesses. Methods: Thus, in this manuscript, we aimed to search, identify, and gather all randomized controlled trials (RCTs) published between 2000-2023 (November) in four major academic databases such as PubMed, ISI Web of Science, Scopus, and ScienceDirect by using a controlled terminology and web strings that reunite six main keywords. We complementarily retrieved data on the ongoing RCTs. Results: Regardless of the relatively high number of results displayed (n = 75), 46.66% (n = 35) were initially deemed eligible after the first evaluation phase after removing duplicates, n = 40 (53.34%). At the second assessment stage, we eliminated 11.42% (n = 4) studies, of which n = 22 finally met the eligibility criteria to be included in the main body of the manuscript. In terms of RCTs, otherwise found in distinct stages of development, n = 3 target FMT and n = 1 probiotics. Conclusions: Although we benefit from the necessary information and technology to design novel strategies for microbiota, only probiotics and synbiotics have been extensively studied in the last decade compared to FMT.

Previous studies have shown observational associations between the gut microbiota and endometriosis; however, the causal nature of such associations remains unclear. This study aimed to analyze the genetic causal relationship between the two.

A gut microbiome genome-wide association study conducted by the MiBioGen consortium was used as exposure data, and summary statistics of endometriosis were obtained from the FinnGen consortium R8 release data. Inverse variance weighted, MR-Egger, weighted median, weighted model, and simple model analyses were applied to examine the causal relationship, and sensitivity analyses were conducted to validate the robustness of the results.

The results showed that, out of 211 gut microbiome taxa, Clostridiales_vadin_BB60_group, Oxalobacteraceae, Desulfovibrio, Haemophilus, and Holdemania had protective effects on endometriosis, while Porphyromonadaceae and Anaerotruncus might contribute to the development of endometriosis. Heterogeneity and pleiotropy analyses confirmed the robustness of the results.

The two-sample Mendelian randomization analysis conducted in this study identified specific intestinal flora with a causal relationship with endometriosis at the genetic level, offering new insights into the gut microbiota-mediated development mechanism of endometriosis.

As an emulsifier and bioactive substance, bile acids (BAs) participate in the absorption of nutrients and in various physiological processes. The objective of this experiment was to investigate the effects of non-12α-hydroxylated BAs (including hyocholic acid, hyodeoxycholic acid and chenodeoxycholic acid, from now on referred to as NBAs) on growth performance, BAs metabolism and the intestinal flora of piglets. The experiment included four groups, with eight piglets per group. The four groups of pigs were fed 0, 60, 120 and 180 mg/kg of NBAs, respectively. The results show that adding NBAs significantly increased the final weight (FW), average daily feed intake (ADFI), average daily gain (ADG), and digestibility of crude fat (EE) and organic matter (OM) in piglets (p < 0.05). Adding NBAs significantly increased the villus height (VH) of the jejunum and ileum (p < 0.05). In addition, NBAs supplementation increased the content of urea nitrogen (BUN) and creatinine (CREA) as well as the ratio of urea nitrogen to creatinine (BUN/CREA) in serum (p < 0.05). Adding NBAs can affect the genes related to BAs enterohepatic circulation. Specifically, adding NBAs significantly decreased the relative mRNA abundance of FXR in the liver (p < 0.05), significantly increased the relative mRNA abundance of CYP27A1 (p < 0.05), and significantly increased the relative mRNA abundance of NTCP (p < 0.05). Adding NBAs also significantly decreased the relative mRNA abundance of FXR in the ileum (p < 0.05). In the full-length 16S rDNA sequencing analysis, ten biomarkers were found from the gate to the species level. NBAs mainly enriched Lactobacillus_Johnsonii and decreased the abundance of Streptococcus_alactolyticus. Short-chain fatty acids (SCFAs) content in the colon was significantly increased (p < 0.05). These results indicate that NBAs supplementation can improve the growth performance of piglets, promote the development of the bile acid replacement pathway and improve intestinal flora.

Previous studies have reported an association between gut microbiota and cirrhosis. However, the causality between intestinal flora and liver cirrhosis still remains unclear. In this study, bi-directional Mendelian randomization (MR) analysis was used to ascertain the potential causal effect between gut microbes and cirrhosis.

Large-scale Genome Wide Association Study (GWAS) data of cirrhosis and gut microbes were obtained from FinnGen, Mibiogen consortium, and a GWAS meta-analysis of Alcoholic cirrhosis (ALC). Two-sample MR was performed to determine the causal relationship between gut microbiota and cirrhosis. Furthermore, a bi-directional MR analysis was employed to examine the direction of the causal relations.

In MR analysis, we found that 21 gut microbiotas were potentially associated with cirrhosis. In reverse MR analysis, 11 gut microbiotas displayed potentially associations between genetic liability in the gut microbiome and cirrhosis. We found that the family Lachnospiraceae (OR: 1.59, 95% CI:1.10-2.29) might be harmful in cirrhotic conditions (ICD-10: K74). Furthermore, the genus Erysipelatoclostridium might be a protective factor for cirrhosis (OR:0.55, 95% CI:0.34-0.88) and PBC (OR:0.68, 95% CI:0.52-0.89). Combining the results from the MR analysis and reverse MR analysis, we firstly identified the Genus Butyricicoccus had a bi-directional causal effect on PBC (Forward: OR: 0.37, 95% CI:0.15-0.93; Reverse: OR: 1.03, 95% CI:1.00-1.05).

We found a new potential causal effect between cirrhosis and intestinal flora and provided new insights into the role of gut microbiota in the pathological progression of liver cirrhosis.

Bile acids (BAs) function as detergents promoting nutrient absorption and as hormones regulating nutrient metabolism. Most BAs are key regulatory factors of physiological activities, which are involved in the regulation of glucose, lipid, and drug metabolisms. Hepatic and intestinal diseases have close connections with the systemic cycling disorders of BAs. The abnormal in BA absorption came up with overmuch BAs could be involved in the pathophysiology of liver and bowel and metabolic disorders such as fatty liver diseases and inflammatory bowel diseases. The primary BAs (PBAs), which are synthesized in the liver, can be transformed into the secondary BAs (SBAs) by gut microbiota. The transformation processes are tightly associated with the gut microbiome and the host endogenous metabolism. The BA biosynthesis gene cluster bile-acid-inducible operon is essential for modulating BA pool, gut microbiome composition, and the onset of intestinal inflammation. This forms a bidirectional interaction between the host and its gut symbiotic ecosystem. The subtle changes in the composition and abundance of BAs perturb the host physiological and metabolic activity. Therefore, maintaining the homeostasis of BAs pool contributes to the balance of the body's physiological and metabolic system. Our review aims to dissect the molecular mechanisms underlying the BAs homeostasis, assess the key factors sustaining the homeostasis and the role of BA acting on host diseases. By linking the BAs metabolic disorders and their associated diseases, we illustrate the effects of BAs homeostasis on health and potential clinical interventions can be taken under the latest research findings.

Chronic liver disease (CLD) is a significant global health burden, leading to millions of deaths annually. The gut-liver axis plays a pivotal role in this context, allowing the transport of gut-derived products directly to the liver, as well as biological compounds from the liver to the intestine. The gut microbiota plays a significant role in maintaining the health of the digestive system. A change in gut microbiome composition as seen in dysbiosis is associated with immune dysregulation, altered energy and gut hormone regulation, and increased intestinal permeability, contributing to inflammatory mechanisms and damage to the liver, irrespective of the underlying etiology of CLD. The aim of this review is to present the current knowledge about the composition of the intestinal microbiome in healthy individuals and those with CLD, including the factors that affect this composition, the impact of the altered microbiome on the liver, and the mechanisms by which it occurs. Furthermore, this review analyzes the effects of gut microbiome modulation on the course of CLD, by using pharmacotherapy, nutrition, fecal microbiota transplantation, supplements, and probiotics. This review opens avenues for the translation of knowledge about gut-liver interplay into clinical practice as an additional tool to fight CLD and its complications.

Whether the World Cancer Research Fund and the American Institute for Cancer Research (WCRF/AICR) dietary recommendations affect the gut microbiota and inflammatory status remains unclear. We examined the association of dietary adherence scores to the WCRF/AICR with gut microbiota and inflammation in a cross-sectional setting.

The WCRF/AICR diet adherence scores were calculated for 151 participants (adenoma 97, non-adenoma 54) from 7-day dietary records. The gut microbiota was analyzed by 16S rRNA gene sequencing of fecal samples. The levels of inflammatory biomarkers in both blood (i.e., IL-6, IL-8, IgA, IgM, and IgG) and fecal samples (i.e., FCP) were evaluated in 97 colorectal adenoma patients who had blood samples available. Multivariable linear regression analyses were conducted to examine the association of individual and total dietary adherence scores with gut microbiota and inflammatory biomarker levels.

Participants with higher adherence had lower relative abundance of Proteobacteria (β = -0.041, 95%CI: -0.073, -0.009), Enterobacteriaceae (β = -0.035, 95%CI: -0.067, -0.003), and unidentified Enterobacteriaceae at the genus level (β = -0.029, 95%CI: -0.055, -0.003) compared to those with lower adherence. Plant-based food intake was positively correlated with increased abundance of Phascolarctobacterium (β = 0.013, 95%CI: 0.001, 0.026). Restricting fast food was linked to high abundance of Bacteroidaceae (β = 0.149, 95%CI: 0.040, 0.257) and Bacteroides (β = 0.149, 95%CI: 0.040, 0.257). Limiting sugary drinks was associated with reduced abundance of Lachnospiraceae (β = -0.155, 95%CI: -0.292, -0.018). Plant-based food intake (β = -0.251, 95%CI: -0.450, -0.052) and restriction of fast food (β = -0.226, 95%CI: -0.443, -0.008) were associated with reduced IGG levels in men. Alcohol restriction was linked to lower IL-6 (β = -7.095, 95%CI: -11.286, -2.903) and IL-8 (β = -7.965, 95%CI: -14.700, -1.230) levels in women, but with higher IL-6 (β = 0.918, 95%CI: 0.161, 1.675) levels in men.

Our findings support the association of adherence to the WCRF/AICR diet with gut microbiota and inflammation. These results need to be validated in additional prospective or interventional studies.

Dihydromyricetin (DMY) is a natural flavonoid with anti-nonalcoholic steatohepatitis (NASH) activity. However, the effects of DMY on the composition of lipids and bile acids (BAs) in serum, and gut microbiota (GM) in ileum of mice with NASH are not clear.

After male C57BL/6 mice was fed with methionine and choline deficiency (MCD) diet and simultaneously administered with DMY (300 mg/kg/day) by gavage for 8 weeks, the pathological changes of liver tissue were observed by Oil Red O, hematoxylin eosin and Masson staining, the levels of serum alaninea minotransferase, aspartate aminotransferase and liver triglyceride, malonic dialdehyde were detected by the detection kits, the composition and contents of serum lipids and BAs were detected by Liquid Chromatograph-Mass Spectrometry, the mRNA levels of hepatic BAs homeostasis-related genes were detected by RT-qPCR, and microbiological diversity in ileum was analyzed by 16S rDNA sequencing.

The results showed that the significant changes including 29 lipids, 4 BAs (23-nor-deoxycholic acid, ursodeoxycholic acid, 7-ketodeoxycholic acid and cholic acid), 2 BA transporters (Mrp2 and Oatp1b2) and 8 GMs between MCD and DMY groups. Among them, DMY treatment significantly down-regulated 21 lipids, 4 BAs mentioned above, the ratio of Firmicutes/Bacteroidota and the abundance of Erysipelotrichaceae, Faecalibacuium, significantly up-regulated 8 lipids and 5 GMs (Verrucomicrobiota, Bacteroidota, Actinobacteria, Akkermansiaceae and Akkermansia).

The results suggested that DMY may alleviate MCD diet-induced NASH through decreasing the serum levels of toxic BAs which regulated by liver Oatp1b2 and Mrp2, regulating the metabolism of related lipids, and up-regulating intestinal probiotics (Actinobacteria and Verrucomicrobiota at the phylum level; Akkermansiaceae at the family level; Akkermansiaat at the genus level) and inhibiting intestinal harmful bacteria (Firmicutes at the phylum level; Erysipelotrichaceae at the family level; Faecalibaculum at the genus level).

Chronic high-fat diet (HFD) consumption causes obesity associated with retention of bile acids (BAs) that suppress important regulatory axes, such as the hypothalamic-pituitary-adrenal axis (HPAA). HFD impairs nutrient sensing and energy balance due to a dampening of the HPAA and reduced production and peripheral metabolism of corticosterone (CORT).

We assessed whether proanthocyanidin-rich grape polyphenol (GP) extract can prevent HFD-induced energy imbalance and HPAA dysregulation.

Male C57BL6/J mice were fed HFD or HFD supplemented with 0.5% w/w GPs (HFD-GP) for 17 weeks.

GP supplementation reduced body weight gain and liver fat while increasing circadian rhythms of energy expenditure and HPAA-regulating hormones, CORT, leptin, and PYY. GP-induced improvements were accompanied by reduced mRNA levels of Il6, Il1b, and Tnfa in ileal or hepatic tissues and lower cecal abundance of Firmicutes, including known BA metabolizers. GP-supplemented mice had lower concentrations of circulating BAs, including hydrophobic and HPAA-inhibiting BAs, but higher cecal levels of taurine-conjugated BAs antagonistic to farnesoid X receptor (FXR). Compared with HFD-fed mice, GP-supplemented mice had increased mRNA levels of hepatic Cyp7a1 and Cyp27a1, suggesting reduced FXR activation and more BA synthesis. GP-supplemented mice also had reduced hepatic Abcc3 and ileal Ibabp and Ostβ, indicative of less BA transfer into enterocytes and circulation. Relative to HFD-fed mice, CORT and BA metabolizing enzymes (Akr1d1 and Srd5a1) were increased, and Hsd11b1 was decreased in GP supplemented mice.

GPs may attenuate HFD-induced weight gain by improving hormonal control of the HPAA and inducing a BA profile with less cytotoxicity and HPAA inhibition, but greater FXR antagonism.

Bile acids (BAs) are well known to facilitate the absorption of dietary fat and fat-soluble molecules. These unique steroids also function by binding to the ubiquitous cell membranes and nuclear receptors. As chemical signals in gut-liver axis, the presence of metabolic disorders such as nonalcoholic fatty liver disease (NAFLD), type 2 diabetes mellitus (T2DM), and even tumors have been reported to be closely related to abnormal levels of BAs in the blood and fecal metabolites of patients. Thus, the gut microbiota interacting with BAs and altering BA metabolism are critical in the pathogenesis of numerous chronic diseases. This review intends to summarize the mechanistic links between metabolic disorders and BAs in gut-liver axis, and such stage-specific BA perturbation patterns may provide clues for developing new auxiliary diagnostic means.

The popularity of plant-based proteins has increased, and mung bean protein (MBP) has gained immense attention due to its high yield, nutritional value, and health benefits. MBP is rich in lysine and has a highly digestible indispensable amino acid score. Dry and wet extractions are used to extract MBP flours and concentrates/isolates, respectively. To enhance the quality of commercial MBP flours, further research is needed to refine the purity of MBPs using dry extraction methods. Furthermore, MBP possesses various biological potential and techno-functional properties, but its use in food systems is limited by some poor functionalities, such as solubility. Physical, biological, and chemical technologies have been used to improve the techno-functional properties of MBP, which has expanded its applications in traditional foods and novel fields, such as microencapsulation, three-dimensional printing, meat analogs, and protein-based films. However, study on each modification technique remains inadequate. Future research should prioritize exploring the impact of these modifications on the biological potential of MBP and its internal mechanisms of action. This review aims to provide ideas and references for future research and the development of MBP processing technology.

Bile acids (BAs) are synthesized in liver tissue from cholesterol and are an important endocrine regulator and signaling molecule in the liver and intestine. It maintains BAs homeostasis, and the integrity of intestinal barrier function, and regulates enterohepatic circulation in vivo by modulating farnesoid X receptors (FXR) and membrane receptors. Cirrhosis and its associated complications can lead to changes in the composition of intestinal micro-ecosystem, resulting in dysbiosis of the intestinal microbiota. These changes may be related to the altered composition of BAs. The BAs transported to the intestinal cavity through the enterohepatic circulation are hydrolyzed and oxidized by intestinal microorganisms, resulting in changes in their physicochemical properties, which can also lead to dysbiosis of intestinal microbiota and overgrowth of pathogenic bacteria, induction of inflammation, and damage to the intestinal barrier, thus aggravating the progression of cirrhosis. In this paper, we review the discussion of BAs synthesis pathway and signal transduction, the bidirectional regulation of bile acids and intestinal microbiota, and further explore the role of reduced total bile acid concentration and dysregulated intestinal microbiota ratio in the development of cirrhosis, in order to provide a new theoretical basis for the clinical treatment of cirrhosis and its complications.