Lactobacillus plantarum AR113 attenuates liver injury in D-galactose-induced aging mice via the inhibition of oxidative stress and endoplasmic reticulum stress

Probiotics could effectively eliminate excess ROS generated during aging or lipid metabolism disorders, but their mechanism is unclear. The major purpose of this study was to investigate the mechanism of L. plantarun AR113 alleviating oxidative stress injury in the D-galactose induced aging mice. The result showed that pretreatment with L. plantarun AR113 significantly relieving H₂O₂ induced cytotoxicity in HepG2 cells by maintain cell membrane integrity and increasing antioxidant enzyme activities. In D-galactose induced aging mice, L. plantarun AR113 could significantly attenuate liver damage and inflammatory infiltration by promoting endogenous GSH synthesis and activating the Nrf2/Keap1 signaling pathway in mice, and increasing the expression of regulated phase Ⅱ detoxification enzymes and antioxidant enzymes. Further analysis shown that gavage of L. plantarun AR113 could significantly reduce the expression of GRP78 and CHOP proteins, and promote the restoration of ER homeostasis, thereby activating cell anti-apoptotic pathways. These results were also confirmed in H₂O₂-treated HepG2 experiments. It indicated that L. plantarun AR113 could inhibit D-galactose-induced liver injury through dual inhibition of ER stress and oxidative stress. L. plantarun AR113 have good application potential in anti-aging and alleviating metabolic disorders.