Exercise fatigue is a phenomenon where the body loses its ability to sustain a specific exercise level or intensity. It arises from multiple factors that negatively impact the body. Although probiotics have been shown to alleviate exercise-induced fatigue, the underlying mechanisms for this effect are not yet fully understood. This study aimed to investigate the anti-fatigue effects of Lactiplantibacillus plantarum SHY21-2 (SHY21-2) in a mouse model and to elucidate the underlying mechanisms. The anti-fatigue effects of SHY21-2 were evaluated by measuring muscle glycogen and serum fatigue markers, with the underlying mechanisms subsequently elucidated through an analysis of mitochondrial function, gut microbiota, and metabolites. The results showed that SHY21-2 significantly enhanced running and swimming endurance, reduced serum fatigue markers including blood levels of lactate (LA), blood urea nitrogen (BUN), and creatine kinase (CK), and increased muscle glycogen levels. It also upregulated mitochondrial biogenesis (peroxisome proliferator-activated receptor-γ co-activator-1α), fusion (mitofusin 2), fission (fission 1), and mitophagy proteins (PTEN induced putative kinase 1, Parkin). SHY21-2 reshaped the gut microbiota, enriching norank_f_Muribaculaceae and Alloprevotella while reducing fatigue-associated genera. Metabolomic analysis revealed 10 upregulated metabolites, including hesperetin and tectorigenin, which were positively correlated with beneficial microbiota. These findings suggest that the anti-fatigue effects of SHY21-2 are associated with enhanced mitochondrial function, as well as with changes in the gut microbiota and host metabolites. This supports its potential as a functional probiotic for endurance improvement.

With the increasing societal pressure, systemic inflammation levels have gradually risen. Probiotics are believed to alleviate stress-related diseases by modulating the gut microbiota. Uncertainty exists about the connection between gut microbiota metabolites and stress-induced inflammation following probiotic therapy. This study investigates whether Lactobacillus (L). pentosus LPQ1 alleviates inflammation caused by chronic unpredictable mild stress (CUMS), and examines its effects on intestinal barrier permeability and gut microbiota metabolites. By increasing colonic tight junction proteins and decreasing inflammatory responses, our findings suggested that intestinal barrier failure and systemic inflammation caused by CUMS are lessened by L. pentosus LPQ1. CUMS-induced alterations in gut microbiota-derived metabolites—particularly inflammation-associated compounds such as melilotussaponin O1, narasin, and (−)-stercobilin—were significantly reversed following treatment with L. pentosus LPQ1. These results imply that metabolites generated by the gut microbiota are important in lowering inflammatory responses associated with CUMS. L. pentosus LPQ1 can effectively alleviate CUMS-exposed inflammatory responses by regulating gut microbiota metabolites and intestinal barrier permeability. This study proposes a gut microbiota-based therapeutic strategy for stress-induced inflammation, potentially paving the way for novel interventions.

Milk and its derivatives are important foodstuffs and are recognized as high-risk categories prone to microbial contamination. Here, we investigated the antibacterial activity and antimicrobial properties of metabolites of Lacticaseibacillus paracasei SHY-X4 isolated from Koumiss in Inner Mongolia. The results showed that the SHY-X4 metabolites had good tolerance to acid (pH = 3), alkali (pH = 9) and heat (105 ℃) treatment and exhibited broad-spectrum antimicrobial activity against a wide range of Gram-positive and Gram-negative pathogens. Further analysis of key antimicrobial components by non-targeted metabolomics revealed 52 potential antimicrobial metabolites (variable importance in prediction (VIP) >1, adjusted P < 0.05, and absolute fold change (FC) >1.3) in SHY-X4, mainly comprising organic acids and peptides. Notably, both physiological and phenotypic perspectives revealed that the inhibitory effect of SHY-X4 metabolites on the growth and biofilm formation of Staphylococcus aureus ATCC25923 and Escherichia coli O157:H7 NCTC12900 positively contributed to the impact on cell viability and metabolic activity, disrupting the integrity of cell membranes and leading to cellular deformation. When applied to the milk models, SHY-X4 metabolites significantly inhibited the growth of pathogens and spoilage bacteria, such as S. aureus, E. coli O157:H7, and Enterobacteriaceae. They also maintained the pH, nutritional composition, and antioxidant activity of pasteurized milk for at least 15 d during refrigerated storage at 4 ℃. Overall, these findings provide insights into the potential application of SHY-X4 metabolites in the dairy industry for combating microbial contamination.

Alcoholic liver disease (ALD) poses a serious threat to public health. Although Lacticaseibacillus paracasei has been shown to mitigate symptoms of ALD, the mechanisms underlying these benefits have yet to be fully elucidated. The purpose of this study was to investigate both the effects and mechanisms of Lacticaseibacillus paracasei DCRFF018 (LP. DCRFF018) on alcohol-induced liver injury. The findings revealed that LP. DCRFF018 administration improved body weight, liver index, and liver function in alcohol-treated mice. Furthermore, LP. DCRFF018 inhibited hepatic lipid accumulation and inflammation by regulating the TLR4/NF-κB, AMPK/SREBP-1, and PPARα signaling pathways. By modulating the TLR4/NF-κB pathway and enhancing tight junction protein expression, LP. DCRFF018 alleviated colonic inflammation and preserved gut barrier integrity. Moreover, supplementing with LP. DCRFF018 regulated the structure and composition of gut microbiota. Notably, supplementation with LP. DCRFF018 significantly increased the relative abundance of Verrucomicrobiota and Akkermansia in alcohol-treated mice, while reducing the relative abundance of norank_f__Oscillospiraceae. Collectively, these findings demonstrate that LP. DCRFF018 improves alcoholic liver injury by regulating the gut microbiota and preserving intestinal barrier function, providing new insights into the management of ALD.