Sodium butyrate ameliorates lipopolysaccharide-induced cow mammary epithelial cells from oxidative stress damage and apoptosis |
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Authors: | Lin Li Huan-Huan Wang Xin-Tian Nie Wan-Ru Jiang Yuan-Shu Zhang |
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Affiliation: | 1. Key Laboratory of Animal Physiology and Biochemistry, College of Veterinary Medicine, Nanjing Agricultural University, Ministry of Agriculture, Nanjing, China;2. Department of Mechanical Engineering, College of Engineering, Nanjing Agriculture University, Nanjing, China |
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Abstract: | This study investigated the molecular mechanism by which sodium butyrate (NaB) causes oxidative stress damage induced by lipopolysaccharide (LPS) on cow mammary epithelial cells (MAC-T). We found that NaB significantly increased the activities of antioxidant enzymes, including superoxide dismutase, glutathione peroxidase, catalase, peroxidase, and total antioxidant capacity and decreased the reactive oxygen species production in LPS-induced MAC-T cells. NaB attenuated protein damage and reduced apoptosis in LPS-induced MAC-T cells. The messenger RNA (mRNA) levels of caspase-3, caspase-9, and Bax decreased, while the Bcl-2 mRNA level increased in LPS-induced MAC-T cells treated with NaB. Our results showed that NaB treatment increased the phosphoinositide 3-kinase (PI3K) and phospho-AKT (P-AKT) protein levels, whereas it decreased the Bax, caspase-3, and caspase-9 protein levels in LPS-induced MAC-T cells. However, the increase in PI3K and P-AKT protein levels and the decrease in Bax, caspase-3, and caspase-9 protein levels induced by NaB treatment were reversed when the cells were pretreated with LY294002 (PI3K inhibitor). These results indicate that NaB ameliorates LPS-induced oxidative damage by increasing antioxidative enzyme activities and ameliorating protein damage in MAC-T cells. In addition, NaB decreased apoptosis by inhibiting caspase-3, caspase-9, and Bax protein levels, and this action was mainly achieved via activation of the PI3K/AKT signaling pathways in LPS-induced MAC-T cells. These results provide substantial information for NaB as a chemical supplement to treat oxidative stress and its related diseases in ruminants. |
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Keywords: | cell apoptosis lipopolysaccharide (LPS) cow mammary epithelial cells (MAC-T) oxidative damage PI3K/AKT signaling pathways sodium butyrate (NaB) |
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