Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic and systemic metabolic liver disease characterized by the presence of hepatic steatosis and at least one cardiometabolic risk factor (CMRF). The pathogenesis of MASLD involves multiple mechanisms, including lipid metabolism disorders, insulin resistance, inflammatory responses, and the hepato-intestinal axis of metabolic dysfunction. Among these factors, diet serves as both an inducement and a potential remedy in the disease's development. Notably, a high-lipid diet exacerbates fat accumulation, oxidative stress, and inflammatory responses, thereby promoting the progression of MASLD. Consequently, dietary induction models have become vital tools for studying the pathological mechanisms of MASLD, providing a foundation for identifying potential therapeutic targets. Additionally, we summarize the therapeutic effects of dietary optimization on MASLD and elucidate the role of specific dietary components in regulating the hepato-intestinal axis, lipid metabolism, and inhibiting inflammatory responses. In conclusion, studies utilizing animal models of MASLD offer significant insights into dietary therapy, particularly concerning the regulation of lipid metabolism-related and hepatoenteric axis-related signaling pathways as well as the beneficial mechanism of probiotics in hepatoenteric regulation. By understanding the specific mechanisms by which different dietary patterns affect MASLD, we can assess the clinical applicability of current dietary strategies and provide new directions for research and treatment aimed at disease modification.

The increased consumption of dietary fats contributes to the development of MAFLD (metabolic fatty liver disease). The ability of broccoli to enhance lipid metabolism has attracted researchers' attention. Researchers fed C57BL/6 mice a 12-week HFD to ensure the induction of MAFLD. The findings indicated that broccoli floret juice could effectively relieve MAFLD. Broccoli is helpful for reducing weight, blood glucose levels, fat accumulation, and insulin resistance associated with MAFLD and reduces the concentrations of TC, TG, LDL-C, GOT, GPT, IL-1β, IL-6, CCL4, and MCP1. Broccoli can increase the concentration of HDL-C, CAT, GSH-Px, SOD, and T-AOC, relieve inflammation and hepatic and ileum damage, and improve the antioxidant capacity of the body. Also, broccoli can optimize the structure of intestinal flora, promote the growth of Allobaculum, Muribaculaceae, Akkermansia, Eubacterium, and Bacteroides, and reduce bile acid deposition. In addition, the FXR/LXRα signaling system is impacted by broccoli, which is capable of raising the average levels of expression of the Fxr, SHP, and Cyp7a1 genes and proteins and reducing those of the genes for Fasn, Lpin 1, Dgat 2, Scd1, LXRα, and SREBP-1c.

Low molecular weight (LMW) thiols, particularly glutathione, play pathogenic roles in various multiorgan diseases. The liver is central for the production and systemic distribution of LMW thiols; thus, it is particularly susceptible to the imbalance of redox status that may determine increased oxidative stress and trigger the liver damage observed in metabolic dysfunction-associated steatotic liver disease (MASLD) models and humans. Indeed, increased LMW thiols at the cellular and extracellular levels may be associated with the severity of MASLD. Here, we present a systematic literature review of recent studies assessing the levels of LMW thiols in MASLD in in vivo and in vitro models and human subjects. Based on the PRISMA 2020 criteria, a search was conducted using PubMed and Scopus by applying inclusion/exclusion filters. The initial search returned 1012 documents, from which 165 eligible studies were selected, further described, and qualitatively analysed. Of these studies, most focused on animal and cellular models, while a minority used human fluids. The analysis of these studies revealed heterogeneity in the methods of sample processing and measurement of LMW thiol levels, which hinder cut-off values for diagnostic use. Standardisation of the analysis and measure of LMW thiol is necessary to facilitate future studies.

Currently, no specific treatment exists to alleviate metabolic dysfunction-associated fatty liver (MAFLD). Previously, Poria cocos (PC) effectively relieved MAFLD, but its bioactive components are still unknown. The bioactive substances in PC that regulate mitochondria function to alleviate MAFLD were thus determined. The L02 hepatocyte model induced by fat emulsion and the MAFLD rat model induced by a high-fat diet (HFD) were developed to explore the efficacy of PC against MAFLD. The activity of PC-derived components in the liver mitochondria of HFD-fed rats was evaluated using the L02 hepatocyte model. Additionally, the PC-derived components from the liver mitochondria were identified by ultra-high performance liquid chromatography/mass spectrometry. Finally, the anti-steatosis ability of PC-derived monomers and monomers groups was evaluated using the adipocyte model. PC maintained the mitochondrial ultrastructure, alleviated mitochondrial oxidative stress, and regulated the energy metabolism and the fatty acid β oxidation to relieve lipid emulsion-induced cellular steatosis and HFD-induced MAFLD. PC-derived components entering the liver mitochondria inhibited oxidative stress injury and improved the energy metabolism to fight cellular steatosis. Additionally, 15 chemicals were identified in the PC-treated rat liver mitochondria. These identified chemical molecules and molecule groups in the mitochondria prevented cellular steatosis by regulating mitochondrial oxidative stress and energy metabolism. PC restores mitochondrial structure and function, alleviating MAFLD, which is related to oxidative stress, energy metabolism, and fatty acid β oxidation. The identified 15 components may be the main effective PC components regulating mitochondria function to alleviate MAFLD. Thus, PC may be a promising mitochondrial regulator to prevent MAFLD.

This study explores the potential therapeutic benefits of using a three-component DGR (composed of specific compounds) to target the NLRP3 inflammasome in the context of non-alcoholic fatty liver disease (NAFLD).

To assess the impact of a three-component DGR on NAFLD, specifically examining its effects on liver lipid accumulation, inflammation, and the diversity of intestinal microbial communities.

NAFLD was induced in 8-week-old Sprague Dawley rats by feeding them a high-fat emulsion diet every morning for 8 consecutive weeks. Oral administration of DGR or its constituent equivalents in the afternoon. The pharmacological effects of DGR were evaluated using H&E, ORO and ELISA methods to determine the changes in serum and liver tissue indexes of rat-models. Immunohistochemical staining and Western blot were used to assess the interaction between DGR, NLRP3 and IL-1β.

The induction of NAFLD resulted in elevated hepatic triglycerides (TG), total cholesterol (TC), and free fatty acids (FFA). However, these alterations were ameliorated upon administration of DGR. It is noteworthy that DGR exhibited superior efficacy in comparison to its constituent compounds, manifesting augmented antioxidant activity, diminished hepatic damage, and the attenuation of pro-inflammatory factors. Both DGR and its individual monomeric constituents exhibited the capacity to attenuate the activation of the NLRP3 inflammasome in the liver, leading to an amelioration of the pathological characteristics associated with NAFLD. An analysis of the intestinal flora unveiled an elevated abundance of p_Firmicutes (1.1-fold), p_Cyanobacteria (5.76-fold), and p_Verrucomicrobia (5.2-fold), accompanied by a heightened p_Firmicutes to p_Bacteroidetes ratio (5.49-fold).

In the non-alcoholic fatty liver disease (NAFLD) rat model, the concurrent administration of three-component DGR effectively regulated lipid deposition, suppressed liver inflammation, and restored balance in the intestinal flora, thereby improving NAFLD pathology. These findings propose a promising therapeutic strategy for NAFLD, centered on inhibiting the NLRP3 inflammasome through the use of the three-component DGR.

Diabetes is a common chronic disease. Chinese herbal medicine (CHM) has a history of several thousand years in the treatment of diabetes, and active components with hypoglycemic effects extracted from various CHM, such as polysaccharides, flavonoids, terpenes, and steroidal saponins, have been widely used in the treatment of diabetes.

Research exploring the potential of various CHM compounds to regulate the mitochondrial respiratory chain complex to improve type 2 diabetes mellitus (T2DM).

The literature data were primarily obtained from authoritative databases such as PubMed, CNKI, Wanfang, and others within the last decade. The main keywords used include "type 2 diabetes mellitus", "Chinese medicine", "Chinese herbal medicine", "mitochondrial respiratory chain complex", and "mitochondrial dysfunction".

Chinese herbal medicine primarily regulates the activity of mitochondrial respiratory chain complexes in various tissues such as liver, adipose tissue, skeletal muscle, pancreatic islets, and small intestine. It improves cellular energy metabolism through hypoglycemic, antioxidant, anti-inflammatory and lipid-modulating effects. Different components of CHM can regulate the same mitochondrial respiratory chain complexes, while the same components of a particular CHM can regulate different complex activities. The active components of CHM target different mitochondrial respiratory chain complexes, regulate their aberrant changes and effectively improve T2DM and its complications.

Chinese herbal medicine can modulate the function of mitochondrial respiratory chain complexes in various cell types and exert their hypoglycemic effects through various mechanisms. CHM has significant therapeutic potential in regulating mitochondrial respiratory chain complexes to improve T2DM, but further research is needed to explore the underlying mechanisms and conduct clinical trials to assess the safety and efficacy of these medications. This provides new perspectives and opportunities for personalized improvement and innovative developments in diabetes management.

Radiation exposure has been linked to the development of brain damage and cognitive impairment, but the protective effect and mechanism of Lycium barbarum pills (LBP) on radiation-induced neurological damage remains to be clarified.

Behavioral tests and immunohistochemical studies were conducted to evaluate the protective effects of LBP extract (10 g/kg orally daily for 4 weeks) against radiation-induced damage on neurogenesis and cognitive function in Balb/c mice exposed to 5.5 Gy X-ray acute radiation.

The results showed that the LBP extract significantly improved body weight loss, locomotor activity and spatial learning and memory. Immunohistochemical tests revealed that the LBP extract prevented the loss of proliferating cells, newly generated neurons and interneurons, especially in the subgranular area of the dentate gyrus.

The findings suggest that LBP is a potential neuroprotective drug for mitigating radiation-induced neuropsychological disorders.

Polygonati Rhizoma (PR), which contains rich national cultural connotations, is a traditional Chinese medicine with homology of medicine and food. It has been used for a long time as a tonic in China's multi-ethnic medical system, and is also used to treat diseases such as premature graying hair, deficiency of blood and essence, diabetes, hypertension, etc. Meanwhile, PR is often used as food in China, India, South Korea and other Asian countries, which can satisfy hunger and provide many health benefits.

This paper systematically reviewed the ethnopharmacology, botany, phytochemistry, pharmacology and related applications research of PR, and provided a reference for the comprehensive applications of PR, including basic research, product development and clinical applications. This paper also refined the national application characteristics of PR, such as rich plant resources, special chemical components and anti-hidden hungry, which laid a foundation for its high value and high connotation development in the future.

The literature information was collected systematically from the electronic scientific databases, including PubMed, Science Direct, Google Scholar, Web of Science, Geen Medical, China National Knowledge Infrastructure, as well as other literature sources, such as classic books of herbal medicine.

A comprehensive analysis of the above literature confirmed that PR has been used in the ethnic medicine system of Asian countries such as China for thousands of years. In this paper, 12 species including official species that can be used as PR are summarized, which provide rich plant resources for PR. The chemical components in PR are divided into nutritional components and active components. The former not only contains non-starch polysaccharides and fructo-oligosaccharides, which account for about 50% in PR and are recognized as high-quality diet in the world, but also contains inorganic elements and mineral elements. And a total of 199 kinds active ingredients, including saponins, flavonoids, alkaloids, etc., were sorted out by us. The above ingredients make PR have a special property of anti-hidden hunger. Studies have shown that PR has a wide range of pharmacological activities, such as immune regulation, blood glucose regulation, lipid-lowering, antioxidant, anti-tumor, antibacterial, etc. It has been widely used in medicine, food, cosmetics, gardens and other fields.

PR, as a classic medicinal material of the same origin, is widely used in the traditional ethnic medicine system. It contains abundant potential plant resources, chemical components and pharmacological activities. This paper also suggests that PR with high application value in food industry, has the potential to become a high-quality coarse grain. Exploring the way of grain and industrialization of PR is beneficial to fully develop the economic value of PR.

Nonalcoholic steatohepatitis (NASH) is among the most common liver diseases in the world. Flavonoids from Scutellaria amoena (SAF) are used in the treatment of hepatopathy in China. However, the effect and mechanism against NASH remain unclear. We investigated the alleviating effect of SAF on NASH via regulating mitochondrial dysfunction and oxidative stress.

The effects of SAF on NASH were evaluated using in vitro and in vivo methods. L02 cells were induced by fat emulsion to establish an adipocytes model, followed by treatment with SAF for 24 h. NASH rat models were established by the administration of a high-fat diet for 12 weeks and were administered SAF for six weeks. Changes in body weight, organ indexes, lipid levels, inflammatory cytokines, mitochondrial indicators, and fatty acid metabolism were investigated.

SAF significantly improved body weight, organ indexes, lipid levels, liver injury, and inflammatory infiltration in NASH rats. SAF notably regulated interleukin-6, tumor necrotic factor-alpha, superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), kelch-like ECH-associated protein 1 (Keap1), nuclear factor-erythroid factor 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1). Additionally, SAF improved mitochondrial dysfunction, increased the levels of GSH, SOD, ATP synthase, complex I and II, and decreased the level of MDA in liver mitochondria. SAF regulated the expression of β-oxidation genes, including peroxisome proliferator-activated receptor -gamma coactivator-1alpha (PGC-1α), carnitine palmitoyltransferase-1 (CPT1) A, CPT1B, medium-chain acyl-CoA dehydrogenase, long-chain acyl-CoA dehydrogenase, very long-chain acyl-CoA dehydrogenase, and PPARα.

SAF can alleviate NASH by regulating mitochondrial function and oxidative stress via the Keap1/Nrf2/HO-1 axis.

Metabolic dysfunction-associated fatty liver disease (MAFLD) is a severe threat to human health. Polygonum multiflorum (PM) has been proven to remedy mitochondria and relieve MAFLD, but the main pharmacodynamic ingredients for mitigating MAFLD remain unclear.

To research the active ingredients of PM adjusting mitochondria to relieve high-fat diet (HFD)-induced MAFLD in rats.

Fat emulsion-induced L02 adipocyte model and HFD-induced MAFLD rat model were used to investigate the anti-MAFLD ability of PM and explore their action mechanisms. The adipocyte model was also applied to evaluate the activities of PM-derived constituents in liver mitochondria from HFD-fed rats (mitochondrial pharmacology). PM-derived constituents in liver mitochondria were confirmed by ultra-high-performance liquid chromatography/mass spectrometry (mitochondrial pharmacochemistry). The abilities of PM-derived monomer and monomer groups were evaluated by the adipocyte model and MAFLD mouse model, respectively.

PM repaired mitochondrial ultrastructure and prevented oxidative stress and energy production disorder of liver mitochondria to mitigate fat emulsion-induced cellular steatosis and HFD-induced MAFLD. PM-derived constituents that entered the liver mitochondria inhibited oxidative stress damage and improved energy production against cellular steatosis. Eight chemicals were found in the liver mitochondria of PM-administrated rats. The anti-steatosis ability of one monomer and the anti-MAFLD activity of the monomer group were validated.

PM restored mitochondrial structure and function and alleviated MAFLD, which may be associated with the remedy of oxidative stress and energy production. The identified eight chemicals may be the main bioactive ingredients in PM that adjusted mitochondria to prevent MAFLD. Thus, PM provides a new approach to prevent MAFLD-related mitochondrial dysfunction. Mitochondrial pharmacology and pharmacochemistry further showed efficient strategies for determining the bioactive ingredients of Chinese medicines that adjust mitochondria to prevent diseases.