Epigallocatechin-3-gallate protects bovine ruminal epithelial cells against lipopolysaccharide-induced inflamm tory damage by activating autophagy  

作　　者：Wanli Zhao Taiyu Shen Bichen Zhao Moli Li Zhaoju Deng Yihui Huo Ben Aernouts Juan J.Loor Androniki Psifidi Chuang Xu 

机构地区：[1]National Key Laboratory of Veterinary Public Health and Safety,College of Veterinary Medicine,China Agricultural University,2 Yuanmingyuan West Road,Beijing 100193,China [2]Department of Biosystems,Division of Animal and Human Health Engineering,KU Leuven University,Kleinhoefstraat 4,Geel 2440,Belgium [3]Department of Animal Sciences,Division of Nutritional Sciences,University of Illinois,Urbana-Champaign,Urbana,IL 61801,USA [4]Department of Clinical Science and Services,Queen Mother Hospital for Animals,The Royal Veterinary College,North Mymms,Hawkshead Lane,Hatfield,Hertfordshire AL97TA,UK

出　　处：《Journal of Animal Science and Biotechnology》2024年第6期2403-2417,共15页畜牧与生物技术杂志(英文版)

基　　金：supported by the National Natural Science Foundation of China(Beijing,China,grant nos.32125038)。

摘　　要：Background Subacute ruminal acidosis(SARA)causes an increase in endotoxin,which can induce immune and inflammatory responses in the ruminal epithelium of dair y 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 coccentrations of tumor necrosis factor(TNF)-αand interleukin-6,and epitheliu m had histological signs of damage.In vitro,immortalized bovine ruminal epithelial cells(BREC)were treated with lipopolysaccharide(LPS)to imitate the inflammatory damage caused by SARA.Our data revealed that BREC treated with 10 pg/mL LPS for 6 h successfully induce a robust inflammatory response as indicated by increased phosphorylation of IKBa and nuclear factor kappa-B(NF-κB)p65.Pre-treatment of BREC with 50μmol/L EGCG for 6 h before LPS challenge promoted the degradation of NLR family pyrin domain containing 3(NLRP3)inflammasome through activation of autophagy,which further repressed activation of NF-κB pathway targeting Toll-like receptor4(TLR4).Analyses 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-in flammatory effects of EGCG help preserve the integrity of the epithelial barrier through activating autophagy when BREC are exposed to LPS.Thus,EGCG could potentially serve as an e,fifective therapeutic agent for SARA-associated inflammation.

关 键 词：Bovine ruminal epithelial cell Epigallocatechin-3-gallate Inflammation Subacute ruminal acidosis 

分 类 号：S858.23[农业科学—临床兽医学]