GABA regulates the proliferation and apoptosis of MAC-T cells through the LPS-induced TLR4 signaling pathway.

Subacute ruminal acidosis (SARA) can cause rapid lipopolysaccharide (LPS) elevation and milk yield decline in lactating ruminants. LPS has been shown to promote apoptosis and reduce the proliferation of mammary epithelial cells. Previous studies have shown that γ- amino butyric acid (GABA) can enhance production performance, regulating β-cell apoptosis and proliferation. Whether GABA can regulate apoptosis and proliferation induced by LPS in mammary epithelial cells is unknown. In this paper, we detected the role of GABA on proliferation and apoptosis as well as inflammation induced by LPS in bovine mammary epithelial cells (MAC-T cell line). In addition, we explored the role mechanism of GABA in LPS-induced MAC-T cells response through detecting the NFκB signaling pathway key molecules. The results suggested that GABA reduced the effects of cell apoptosis induced by LPS. Furthermore, GABA inhibited the expression of inflammatory cytokines activated by LPS. More importantly, blocking GABA receptors with its antagonist, GABA could not reduce the expression of inflammatory and pro-apoptotic factors activated by LPS. Notably, GABA significantly decreased the TLR4, NFκB p65, and MyD88 mRNA expression levels that were elevated by LPS. Our data indicated that GABA can improve cell viability and decrease apoptosis induced by LPS, while exerting an anti-inflammatory effect through the NFκB signaling pathway.