Effect of Limosilactobacillus fermentum CQPC08 on Regulating Oxidative Stress and Exercise Capacity

In this study, a mouse model of oxidative stress was established by D-galactose induction to investigate the effects of Limosilactobacillus fermentum CQPC08(LF-CQPC08) on hepatic oxidative stress and exercise endurance. The exercise capacity of mice was evaluated using an exhaustive running test. Relevant biomarkers in serum and liver tissue were measured using assay kits, and hepatic histopathology was observed via hematoxylin and eosin(H&E) staining. Additionally, quantitative polymerase chain reaction(qPCR) was employed to determine the mRNA expression levels of specific genes in the liver tissue, gastrocnemius muscle tissue, and intestinal contents. The results indicated that, compared with the model group, LF-CQPC08 intervention significantly prolonged the exhaustive running time (49.5±5.3 min) of mice. It reduced serum levels of lactic acid(LA, 4.99±0.28 mmol/L), creatine kinase(CK, 336.79±35.05 U/L), and lipopolysaccharide(LPS, 0.18±0.02 pg/mL), while increasing the reserves of hepatic glycogen(HG, 10.87±1.57 mg/g) and muscle glycogen(MG, 1.65±0.20 mg/g). Furthermore, it decreased the levels of tumor necrosis factor-alpha(TNF-α, 74.56±8.62 pg/mg), interleukin-6(IL-6, 80.14±7.71 pg/mg), and reactive oxygen species(ROS, 4.54±0.22×10³ RFU fluorescence intensity). Histopathological examination of liver sections revealed that LF-CQPC08 alleviated oxidative stress-induced tissue damage. Further molecular analyses demonstrated that LF-CQPC08 up-regulated the mRNA expression of superoxide dismutase 1(SOD1), SOD2, catalase(CAT), and glutathione peroxidase 4(GPx4) in the liver and gastrocnemius muscle of mice subjected to exhaustive exercise under oxidative stress. Additionally, LF-CQPC08 also upregulated the protein expression of SOD2 and CAT in the gastrocnemius tissue of oxidatively damaged mice. Analysis of intestinal contents showed that LF-CQPC08 increased the relative abundance of Bifidobacterium, Lactobacillus, Eubacterium rectale, Faecalibacterium prausnitzii, and Clostridium in model mice, while decreasing the relative abundance of Enterococcus and Desulfovibrio. Notably, it significantly elevated the relative abundance of Lactobacillus to a level even higher than that in the normal group. These findings suggest that LF-CQPC08 possesses the potential to mitigate oxidative damage and improve physical endurance.