Abstract
Background Subacute ruminal acidosis(SARA)causes an increase in endotoxin,which can induce immune and inflammatory responses in the ruminal epithelium of dairy cows.In non-ruminants,epigallocatechin-3-gallate(EGCG),a major bioactive ingredient of green tea,is well-known to alleviate inflammation.Whether EGCG confers protection against SARA-induced inflammation and the underlying mechanisms are unknown.Results In vivo,eight ruminally cannulated Holstein cows in mid-lactation were randomly assigned to either a low-concentrate(40％)diet(CON)or a high-concentrate(60％)diet(HC)for 3 weeks to induce SARA(n=4).Cows with SARA had greater serum concentrations of tumor necrosis factor(TNF)-α and interleukin-6,and epithelium had histological signs of damage.In vitro,immortalized bovine ruminal epithelial cells(BREC)were treated with lipopoly-saccharide(LPS)to imitate the inflammatory damage caused by SARA.Our data revealed that BREC treated with 10 μg/mL LPS for 6 h successfully induce a robust inflammatory response as indicated by increased phosphoryla-tion of IKBα and nuclear factor kappa-B(NF-κB)p65.Pre-treatment of BREC with 50 μmol/L EGCG for 6 h before LPS challenge promoted the degradation of NLR family pyrin domain containing 3(NLRP3)inflammasome through acti-vation of autophagy,which further repressed activation of NF-κB pathway targeting Toll-like receptor 4(TLR4).Analy-ses also revealed that the ECGG upregulated tight junction(TJ)protein expression upon incubation with LPS.Conclusions Subacute ruminal acidosis causes ruminal epithelium injury and systemic inflammation in dairy cows.However,the anti-inflammatory effects of EGCG help preserve the integrity of the epithelial barrier through activat-ing autophagy when BREC are exposed to LPS.Thus,EGCG could potentially serve as an effective therapeutic agent for SARA-associated inflammation.
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