Lactobacillus rhamnosus GR-1 alleviates Escherichia coli-triggered bovine endometrial epithelial cells damage via the ROS-mitochondrial pathway.

Abstract

Objective: The objective of this study was to evaluate the function of the reactive oxygen species (ROS)-mitochondrial pathway in attenuating Escherichia coli (E. coli) induced apoptosis in bovine endometrial epithelial cells (BENDs) by Lactobacillus rhamnosus (L. rhamnosus) GR-1.

Methods: The BENDs were exposed to preincubation with and without L. rhamnosus GR-1 for 3 hours (h) and they were later subject to E. coli for 6 h. The release of lactate dehydrogenase (LDH), the expression of oxidative factors, the expression of mitochondrial membrane potential (MMP), apoptotic rate and apoptosis-associated protein expression were observed. Then, ROS expression, MMP level and cell rate apoptosis rate were further detected after the intervention of antioxidant n-acetyl-l-cysteine (NAC).

Results: L. rhamnosus GR-1 was capable of obviously alleviating the content of LDH, ROS expression, the apoptotic rate and MDA concentrations in BENDs induced by E. coli (p<0.01). In addition, L. rhamnosus GR-1 could notably promote the levels of antioxidant factors (SOD, GSH, T-AOC) (p<0.01), inhibit the depolarization of MMP (p<0.01), and levels of apoptosis-related factors (Bax, Caspase-3 and Cyt-c), and promote anti-apoptosis factor (Bcl-2) (p<0.01). Moreover, after the intervention of antioxidant NAC, ROS expression, MMP depolarization, and apoptotic rate induced by E. coli in BENDs were decreased (p<0.01).

Conclusion: In E. coli-induced apoptosis in BENDs, therapeutic strategies aimed at down-regulating ROS and MDA and up-regulating antioxidant factors may maintain mitochondrial function and provide theoretical support for the use of probiotics in bovine endometritis.