Sodium butyrate ameliorates lipopolysaccharide‐induced cow mammary epithelial cells from oxidative stress damage and apoptosis

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.

Dandelion Extract Alleviated Lipopolysaccharide-Induced Oxidative Stress through the Nrf2 Pathway in Bovine Mammary Epithelial Cells

“…Then TLR4 initiates the activation of nuclear factor κB (NF-κB), which enhances the production of proinflammatory cytokines and leads to subsequent oxidative stress [ 4 , 5 ]. Intramammary administration with lipopolysaccharide (LPS) stimulated inflammatory response and caused subsequent oxidative damage to the mammary gland through the activation of transduction pathways that express proinflammatory cytokines [ 6 ].…”

Matrine-chitosan hydrogels for treating subclinical bovine mastitis by intramammary infusion—effect on milk microbiome and metabolites

“…Previous research found that bacterial invasion can induce in ammatory reactions and cause oxidative damage during the development of the breast [33], accompanied by apoptosis . [34,35]. The reduction in sphingolipids, glycerolipids, and fatty acyls seen in this study indicates that apoptosis caused by in ammatory reactions may have been weakened.…”

Sodium butyrate protects against high-fat diet-induced oxidative stress in rat liver by promoting expression of nuclear factor E2-related factor 2

“…Oxidative stress induces insulin resistance by impairing insulin signal transduction (36) . Previous studies have shown that administering NaB attenuates oxidative stress in many tissues (37,38) and cells (39) . PI3K and p-AKT play key roles in insulin signalling pathway.…”

“…PI3K and p-AKT play key roles in insulin signalling pathway. NaB increases PI3K and p-AKT protein levels (39) and alleviates the oxidative status in sub-acute ruminal acidosis through partial activation of antioxidant enzyme genes (37) . In agreement with these previous findings, we found that NaB restored the hepatic expression of IRS1, PI3K and p-AKT that was down-regulated by high-fat diet.…”