Oxidative stress occurs in a variety of clinical liver diseases and causes cellular damage and mitochondrial dysfunction. The clearance of damaged mitochondria by mitophagy may facilitate mitochondrial biogenesis and enhance cell survival. Although the supplementation of docosahexaenoic acid (DHA) has been recognized to relieve the symptoms of various liver diseases, the antioxidant effect of DHA in liver disease is still unclear. The purpose of our research was to investigate the antioxidant effect of DHA in the liver and the possible role of mitophagy in this. In vitro, H₂O₂-induced injury was caused in AML12 cells. The results showed that DHA repressed the level of reactive oxygen species (ROS) induced by H₂O₂ and stimulated the cellular antioxidation response. Most notably, DHA restored oxidative stress-impaired autophagic flux and promoted protective autophagy. In addition, PINK/Parkin-mediated mitophagy was activated by DHA in AML12 cells and alleviated mitochondrial dysfunction. The ERK1/2 signaling pathway was inhibited during oxidative stress but reactivated by DHA treatment. It was proven that the expression of ERK1/2 was involved in the regulation of mitophagy by the ERK1/2 inhibitor. We further proved these results in vivo. DHA effectively alleviated the liver oxidative damage caused by CCl₄ and enhanced antioxidation capacity; intriguingly, autophagy was also activated. In summary, our data demonstrated that DHA protected hepatocytes from oxidative damage through GPR120/ERK-mediated mitophagy.

Sodium butyrate (SB) is reported to regulate lipid metabolism in mammals, and the relationship between maternal nutrition and offspring growth has drawn much attention in the last several years. To elucidate the effects of maternal dietary SB supplementation on hepatic lipid metabolism in weaning rats, we fed 16 primiparous purebred female SD rats either a chow-diet or a 1 % sodium butyrate diet throughout pregnancy and lactation. At weaning age, samples of the maternal subcutaneous adipose tissue and offspring liver were taken. The serum indexes and expressions of proteins related to lipid metabolism were detected in the mother and offspring, respectively. The results showed that the maternal SB supplement increased the concentration of non-esterified fatty acid (NEFA) in the maternal and offspring serum (P < 0.05). Total cholesterol (Tch) increased significantly in the weaning-rat serum (P < 0.05). Maternal adipose tissue from the SB-supplemented rats showed higher content of protein G-coupled protein (GPR43) and protein kinase A (PKA) (P < 0.05). The expression of protein adipose triglyceride lipase (ATGL), and of total and phosphorylated hormone sensitive lipase (HSL), in the maternal adipose tissue increased significantly (P < 0.05) compared to the control group. However the proteins related to lipogenesis showed no significant changes. Moreover, the concentration of triglyceride in the offspring liver increased significantly, and this likely resulted from an increase in the levels of fatty acids binding protein (FABP) and fatty acid translocase (CD36) protein (P < 0.05). SB exposure during pregnancy and lactation increased the hepatic total cholesterol (Tch) content (P < 0.01), which was related to a significantly up-regulated offspring hepatic expression of low density lipoprotein receptor (LDLR) protein (P < 0.05). These results indicate that a maternal SB supplement during pregnancy and the lactation period promotes maternal fat mobilization, which may result in fatty acid uptake and lipid accumulation in the liver of the offspring.

Microplastics (MPs), environmental pollutants resulting from the degradation of plastic products and industrial processes, have become ubiquitous in global ecosystems. MPs can enter the human body through ingestion, inhalation, and dermal contact subsequently accumulating in vital tissues such as the liver, lungs, blood, and placenta. This review systematically evaluates the metabolic fate of MPs in humans, emphasizing their translocation across biological barriers and organ-specific deposition. We elaborated on the direct damage of MPs on the intestinal mucosal barrier and while simultaneously remodelling the gut microbiota, and focuses on the regulatory role of gut microbiota in the process of MPs-induced human health damage. Ingestion of MPs induces mechanical damage to the intestinal mucosa, epithelial cell apoptosis, and inflammation. It also alters gut microbial composition, that most notably increasing Firmicutes while decreasing Bacteroidetes and Actinobacteria, as well as disrupts metabolite production, including short-chain fatty acids and bile acids. These microbiota-mediated changes propagate via the gut-liver or gut-brain axis, contributing to obesity, cardiovascular diseases, neurological disorders, and reproductive impairments. This review clarifies the potential mechanism of MPs affecting human health through gut microbiota, and clearly identifies gut microbiota regulation as a potential therapeutic strategy to mitigate MP-induced diseases, and provides practical guidance for reducing MP-related health risks.

Heat stress is one of the key factors affecting broiler production. This study aimed to investigate the protective effects and underlying mechanisms of chromium propionate (CrP) against heat stress in broilers. A total of 180 yellow-feathered broilers were randomly divided into 3 groups, with 6 replicates per group and 10 broilers per replicate. The CON and HS groups were fed with a basic diet, while the PAC group was supplemented with 0.2 mg/kg CrP. Following pre-feeding for 7 days, HS and PAC groups were exposed to cyclic HS (8 h at 30, 32, and 34 °C, respectively) for two weeks, while the control group was maintained at 26 ℃ ± 1 ℃. The experiment was designed in accordance with a randomized block design, and data were analyzed by one-way ANOVA. The results demonstrated that dietary supplementation with CrP eased heat stress–induced reductions in BW and ADG as well as increased the feed conversion ratio. Heat stress considerably decreased gut length and V/C across all intestinal segments. Moreover, CrP suppressed heat stress–induced increases in serum corticosterone and lipopolysaccharide levels while enhancing intestinal glutathione peroxidase activity. Gene expression analysis of jejunal mucosa revealed that CrP downregulated heat stress-induced upregulation of heat shock proteins and inflammation-related genes COX2 and NLRP3 while enhancing the expression of Mucin2 , Occludin and ZO-1 . Analysis of 16S rRNA sequencing revealed distinct differences in microbial composition and potential functional shifts among groups. At the genus level, heat stress decreased Alistipes relative abundance along with marked increases in Lactobacillus count; conversely, CrP reversed these trends. LEfSe identified Lactobacillus and Parabacteroides as the predominant bacteria in the HS group, while Gemmatimonas and Cetobacterium predominated the PAC group. Functional prediction analyses indicated that heat stress suppressed carbohydrate and amino acid metabolism while enhancing RNA degradation pathways; these effects were effectively reversed by CrP supplementation. Further correlation analyses revealed positive associations between Alistipes and BW, ADG and ADFI, and negative correlations with HSPs . By contrast, Lactobacillus and Parabacteroides were negatively correlated with BW and ADG, and positively correlated with HSPs . In conclusion, dietary supplementation with CrP considerably enhances growth performance, promotes intestinal repair and restores homeostasis in heat-stressed broilers.