Taurine alleviates oxidative stress, inflammation, and mitochondrial apoptosis in lipopolysaccharide-induced bovine endometrial epithelial cells by activating nrf2/HO-1 and inhibiting TLR4-mapk/NF-κb and Caspase-3 pathways.

Bovine endometritis negatively impacts reproductive performance and causes significant economic losses in the dairy industry. Taurine is known for its antioxidant and anti-inflammatory properties; however, its protective roles in bovine endometritis remain unclear. This study aimed to investigate the protective effects of taurine against injury in lipopolysaccharide (LPS)-induced bovine endometrial epithelial cells. The results confirmed that taurine treatment protected LPS-induced cells in a time- and dose-dependent manner. First, oxidative stress was alleviated by increasing the activities of superoxide dismutase and glutathione, as well as upregulating protein expression in the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway, while decreasing levels of malondialdehyde and reactive oxygen species. Second, inflammation was reduced by suppressing mRNA expression of Toll-like receptor 4 (TLR4) and proinflammatory cytokines, and by decreasing phosphorylation of extracellular signal-regulated kinase, p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, inhibitor of kappa B alpha, and nuclear factor kappa B p65 subunit in the nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. Third, mitochondrial apoptosis was mitigated by restoring mitochondrial membrane potential and modulating apoptosis-related protein levels. Overall, taurine acts as a natural protective agent against LPS-induced damage in bovine endometrial epithelial cells through its antioxidant, anti-inflammatory, and anti-apoptotic effects via modulation of the Nrf2/HO-1, TLR4-MAPK/NF-κB, and cysteine-aspartic acid protease-3 pathways. These findings highlight taurine's potential as a therapeutic agent for bovine endometritis.