Alcohol-related liver injury is a widespread global health concern caused by chronic excessive alcohol consumption, with inflammation serving as the central mechanism driving disease progression. Although contemporary medical interventions offer diverse therapeutic options for alcohol-related liver disease (ALD), their efficacy is limited and may induce undesirable adverse effects. Probiotics, prebiotics, synbiotics, and postbiotics have emerged as promising therapeutic strategies due to their food-grade safety and anti-inflammatory properties. To date, there remains a lack of a comprehensive review on the impact of these biotic interventions on alcohol-related liver injury. This review examines how the metabolic byproducts generated during alcohol metabolism trigger inflammatory responses and explores the potential mechanisms linking inflammation to the progression of ALD. It also highlights that probiotics, prebiotics, synbiotics, and postbiotics represent promising therapeutic strategies due to their food-grade safety and anti-inflammatory properties.

Lactiplantibacillus plantarum 104, which was previously screened in the laboratory, has been confirmed to have the effect of lowering lipids and regulating intestinal microbial homeostasis. However, the mechanism of action of its fermentation supernatant in alleviating metabolic disorders is unclear. L. plantarum 104 cell-free supernatant (LP104s) was fed to high-fat diet C57BL/6N mice for 8 weeks. The intervention of LP104s increased the concentration of conjugated bile acids in the ileum, especially taur-α/β-muricholic acid sodium salt (T-α-MCA or T-β-MCA), inhibited intestinal farnesoid X receptor (FXR) -related signaling pathways. LP104s reduced cholesterol levels by increasing the synthesis of hepatic cholic acid (CA), chenodeoxycholic acid (CDCA), and the excretion of bile acids in feces. Moreover, Western blotting results showed that TLR2/NF-κB signaling pathway expression was inhibited. In addition, 16S rRNA sequencing results showed that LP104s regulated the relative abundance of bacteria associated with inflammatory response and obesity (Prevotella, Ruminococcus, and Clostridium). Therefore, this paper further elaborates the role of gut microbiology and bile acids in improving metabolism from the perspective of secondary bile acids and intestinal chronic inflammation and also lays a theoretical foundation for the next step in the development of fermentation products of this strain.

The gut microbiota and it’s metabolism are vital targets of probiotics regulating high fat-diet (HFD) induced hyperlipidemia, which can relieve the pressure caused by the striking growth of sub-health people. Pediococcus pentosaceus PP04 (PP04) could colonize in intestine to regulate gut microbiota and it’s metabolites directly, the rebalanced intestinal flora mediated by PP04 could facilitate the secretion of short chain fatty acids to control body weight gain, PP04 intervention also changed bile acid (BA) profiles and enhanced the ileal concentrations of antagonists including tauro-α/β-muricholic acid sodium salt and ursodeoxycholic acid to inhibit intestinal farnesoid X receptor/fibroblast growth factor 15 (FXR/FGF15) signaling coupled with the activation of hepatic FXR/small heterodimer partners signaling, which accelerated the hepatic BA de novo synthesis and excretion with feces to eliminate HFD caused hyperlipemia effectively. This study provided important evidence regarding PP04 as dietary supplement to relieve hyperlipidemia by influencing BA enterohepatic circulation.

This study aimed to investigate the effect of ginseng glucosyl oleanolate (GGO) on non-small cell lung cancer (NSCLC) both in vitro and in vitro. GGO significantly inhibited the proliferation of A549 cells and tumor growth of A549-xenograft nude mice. Metabonomics analysis showed that GGO treatment changed the metabolites of glycolysis and TCA cycle, which was consistent with KEGG enrichment analysis of transcriptomics. GGO inhibited the expression of glutaminase (GLS), decreased the content of glutamic acid and the carbon input of the TCA cycle, and finally significantly blocked the production of ATP. Meanwhile, GGO treatment decreased the levels of glutathione (GSH) and glutathione peroxidase (GSH-PX), increased the accumulation of Fe²⁺ and malondialdehyde (MDA), downregulated solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4) protein expression, which led to the redox imbalance and induced ferroptosis in A549 cells and tumor tissue. These findings provided compelling evidence that GGO may represent a potential new approach to treating NSCLC.

Trehalose (TRE) was used to improve the gastrointestinal tolerance of Lactobacillus plantarum embedded with whey protein concentrate/pullulan (WPC/PUL) hydrogel and the embedded L. plantarum was applied to juice. The study indicated that 5% TRE significantly increased the viable counts of L. plantarum embedded in WPC/PUL hydrogel from (8.83 ± 0.03) to (9.14 ± 0.04) (lg (CFU/g)) in simulated gastric juice (SGJ) and from (9.13 ± 0.04) to (9.38 ± 0.04) (lg (CFU/g)) in simulated intestinal juice, respectively. The addition of TRE improved the glass transition temperature of WPC/PUL hydrogel and decreased the hardness and its solubility in SGJ, which may be responsible for the improved protection of WPC/PUL hydrogels on L. plantarum. In addition, TRE increased the viable counts of L. plantarum in WPC/PUL probiotic microcapsule juice at low pH and high temperature during storage.