Efficacy of sodium butyrate in alleviating mammary oxidative stress induced by sub-acute ruminal acidosis in lactating goats.

Sub-acute ruminal acidosis (SARA) [1] is one of the most common problems of dairy animals causing great economical loss due to decreased milk production. Here we determined the antioxidant effect of sodium butyrate (NaB) [2] in experimentally induced SARA and its effects on mammary epithelial tissues of goat. Goats (n = 12) were equally divided into two groups: high-concentrate (HC) as control group fed with HC diet (concentrate: forage = 6:4) whereas HC + NaB as treatment group fed HC diet with NaB at 1% by weight for 24 weeks. Mammary epithelial tissue samples were analyzed for the expression of genes and proteins responsible for oxidative stress as well as biochemical markers of antioxidant activity in the form of Reactive Oxygen Species (ROS). The total antioxidant capacity (T-AOC) of antioxidant enzymes was also calculated. Butyrate induced antioxidant effect by increasing mRNA and protein abundance of antioxidants in mammary gland of HC + NaB group compared to HC group. Likewise, the total antioxidant capacity (T-AOC) was significantly increased and Malondialdehyde (MDA) concentration was decreased in HC + NaB group compared to HC group. It is concluded that oxidative stress in mammary gland of goats induced by high concentrate diet was alleviated by NaB supplementation.

Microbial community shifts elicit inflammation in the caecal mucosa via the GPR41/43 signalling pathway during subacute ruminal acidosis.

BACKGROUND: Dietary structure in ruminants is closely connected with the composition of gastrointestinal microbiota. Merging study has shown that dietary induced SARA causes the alteration of microbial community in the cecum leading to the local inflammation. However, the mechanisms of cecum inflammation elicited by the shift of microbial flora in ruminants are largely unknown, and whether the development of this inflammation is modified by epigenetic modifications. RESULTS: Ten multiparous lactating goats were randomly seperated into two groups and received either a low concentrate diet (LC, 40% concentrate, n = 5) or a high concentrate diet (HC, 60% concentrate) to induce subacute ruminal acidosis (SARA). Compared with LC, HC-induced SARA altered the predominant phyla and genera, thereby increasing the concentration of lipopolysaccharide (LPS) and short chain fatty acids (SCFAs). Meanwhile, HC-induced SARA enhanced the mRNA expression of cytokines and chemokines and the expression of mRNA and protein of GPR41, GPR43, p38 and ERK1/2, while HC-induced SARA had no effect on TLR4 and p65. Furthermore, HC-induced SARA decreased the percentage of chromatin compaction and DNA methylation at the area of the promoters of GPR41 and GPR43. CONCLUSION: This study indicated that HC diet induced SARA resulted in the alteration in the composition of cecal microbiota. This alteration increased the concentration of LPS, but failing to activate TLR4 signaling pathway due to the tolerance effect of intestinal epithelial cell to certain level of LPS, as well as elevated the concentration of SCFAs, thereby activating GPR41 and GPR43 signaling pathway to produce cytokines and chemokins and cause the cecal inflammation. And epigenetic mechanisms contributed to the development of this inflammation in the lactating goats suffering from SARA.

Sodium Butyrate Mitigates iE-DAP Induced Inflammation Caused by High-Concentrate Feeding in Liver of Dairy Goats.

The aim of this study is to explore the impact of sodium butyrate on d-glutamyl- meso-diaminopimelic acid (iE-DAP)-induced liver inflammation in dairy goats during subacute ruminal acidosis (SARA) caused by high-concentrate feed. To achieve this aim, 12 lactating dairy goats were randomly divided into two groups: a high-concentrate feed group ( n = 6, concentrate/forage = 6:4) as the control group and a sodium butyrate (SB) with high-concentrate feed group ( n = 6, concentrate/forage = 6:4, with 1% SB by wt.) as the treatment group. A rumen pH below 5.6 lasted for at least 4 h/d due to long-term HC feeding. The concentration of iE-DAP was significantly lower (11.67 ± 3.85 µg/mL, and 7.74 ± 1.46 µg/mL, at the fourth h and sixth h of feeding, respectively) in the SB-treated group than that in the HC group (51.45 ± 5.71 µg/mL, and 18.31 ± 3.83 µg/mL, at the fourth h and sixth h of feeding, respectively). Meanwhile, SB significantly suppressed the mRNA expression of inflammatory genes (NOD1, RIPK2, TAK1, NF-κB/p65, ERK, JNK2, p38, IL-1ß, TNF-α, CCL5, CCL20, CXCL12, FOS, ß-defensin/LAP). Moreover, the protein expression of NOD1, p-IκBα, p-NF-κB/p-p65, p-ERK1/2, p-JNK, p-p38, and HDAC3 was significantly downregulated in the HC+SB group. In conclusion, iE-DAP-induced inflammation and liver disruption generated by the HC diet was mitigated by SB treatment.