NOD1/NF-κB signaling pathway inhibited by sodium butyrate in the mammary gland of lactating goats during sub-acute ruminal acidosis.

Animals nurtured with a high-concentrate diet for a more extended period can cause subacute ruminal acidosis (SARA). In this study, twelve mid-lactating goats were separated into two groups (n = 6): a high concentrate diet (HC) control and a high concentrate with buffer (HCB) treatment group. Rumen fistula was installed in all lactating goats in the 14th week of the experiment. Goats were slaughtered in the 24th week. Our results showed that a pH value < 5.8 sustained at different periods of time for more than 3 h/day in the group HC, which confirms that SARA was prompted efficiently. Additionally, the group HCB exhibited lower concentration of LPS in peripheral blood than the group HC. Radioimmunoassay revealed a substantial reduction in the concentration level of proinflammatory cytokines in the lacteal blood of the group HCB compared to group HC. The transcriptional profiles in mammary gland following different treatments showed a significant decrease in the expression of NOD1, IKβ, and NF-κB in HCB group, followed by a decreased transcriptional level of (TNF-α, IL-1β and IL-6). Our research explores that HC diet nurtured to lactating goats for a more extended period can induce SARA by increasing the LPS and proinflammatory cytokine concentrations in plasma, that ultimately triggers the NOD1/NF-κB inflammatory pathway and induce mammary cell inflammation. Additionally, oral supplementation of sodium butyrate can decrease the concentrations of LPS and proinflammatory cytokines and inhibits NOD1/NF-κB inflammatory pathway.