Abstract: Objective: To analyze the mechanism by which Lactobacillus paracasei FM-M9-1 repairs oxidative damage in mice. Methods: A mouse model of oxidative damage was induced by D-galactose. The model mice were gavaged with strain FM-M9-1 at low and high doses of (5.01 ± 0.05) × 1010 and (5.01 ± 0.05) × 108 CFU/mL for 60 successive days, separately. Vitamin C was used as a positive control drug. Afterwards, the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the contents of malondialdehyde (MDA) and protein carbonyl groups in renal and hepatic tissues were measured. We also examined the expression levels of Sod, Gsh-Px, Nrf2 and Trx by real-time fluorescent quantitative polymerase chain reaction (qPCR). Results: The administration of FM-M9-1 significantly enhanced SOD and GSH-Px activities and reduced MDA and protein carbonyl contents. At the transcriptional level, qPCR analysis suggested that the gene expression of Sod, Gsh-Px, Nrf2 and Trx in mice administered with FM-M9-1 increased. Conclusion: Strain FM-M9-1 can alleviate oxidative stress by increasing the activities of antioxidant enzymes, inhibiting lipid and protein oxidation, and up-regulating the expression of antioxidant function-related genes. Overall, strain FM-M9-1 is a promising probiotic candidate for application in functional foods and antioxidant supplements.

Key words: Lactobacillus paracasei, D-galactose, mice, oxidative damage, repair mechanism