L.reuteri ZJ617 inhibits inflammatory and autophagy signaling pathways in gut-liver axis in piglet induced by lipopolysaccharide

作     者：Tao Zhu Jiangdi Mao Yifan Zhong Congxiang Huang Zhaoxi Deng Yanjun Cui Jianxin Liu Haifeng Wang Tao Zhu;Jiangdi Mao;Yifan Zhong;Congxiang Huang;Zhaoxi Deng;Yanjun Cui;Jianxin Liu;Haifeng Wang

作者机构：The Key Laboratory of Molecular Animal NutritionMinistry of EducationCollege of Animal ScienceZhejiang UniversityHangzhou 310058China Xixi Hospital of HangzhouHangzhou 310023China 

出 版 物：《Journal of Animal Science and Biotechnology》 (畜牧与生物技术杂志（英文版）)

年 卷 期：2022年第13卷第2期

页      面：551-566页

核心收录：

学科分类：090603[农学-临床兽医学] 0905[农学-畜牧学] 09[农学] 0906[农学-兽医学] 

基　　金：This study was supported by the National Natural Science Foundation of China(31672430) the National Key Research and Development Program of China(2017YFD0500502) the Natural Science Foundation of Zhejiang Province(Z19C170001). 

主　　题：Gut-liver axis Hepatic injury Intestinal barrier Lactobacillus Piglet Signaling pathways 

摘      要：Background:This study investigated the protective effects of L.reuteri ZJ617 on intestinal and liver injury and the underlying mechanisms in modulating inflammatory,autophagy,and apoptosis signaling pathways in a piglet challenged with lipopolysaccharide(LPS).Methods:Duroc×Landrace×Large White piglets were assigned to 3 groups(n=6/group):control(CON)and LPS groups received oral phosphate-buffered saline for 2 weeks before intraperitoneal injection(i.p.)of physiological saline or LPS(25μg/kg body weight),respectively,while the ZJ617+LPS group was orally inoculated with ZJ617 for 2 weeks before i.***.of LPS.Piglets were sacrificed 4 h after LPS injection to determine intestinal integrity,serum biochemical parameters,inflammatory signaling involved in molecular and liver injury pathways.Results:Compared with controls,LPS stimulation significantly increased intestinal phosphorylated-p38 MAPK,phosphorylated-ERK and JNK protein levels and decreased IκBαprotein expression,while serum LPS,TNF-α,and IL-6 concentrations(P0.05)increased.ZJ617 pretreatment significantly countered the effects induced by LPS alone,with the exception of p-JNK protein levels.Compared with controls,LPS stimulation significantly increased LC3,Atg5,and Beclin-1 protein expression(P0.05)but decreased ZO-1,claudin-3,and occludin protein expression(P0.05)and increased serum DAO and D-xylose levels,effects that were all countered by ZJ617 pretreatment.LPS induced significantly higher hepatic LC3,Atg5,Beclin-1,SOD-2,and Bax protein expression(P0.05)and lower hepatic total bile acid(TBA)levels(P0.05)compared with controls.ZJ617 pretreatment significantly decreased hepatic Beclin-1,SOD2,and Bax protein expression(P0.05)and showed a tendency to decrease hepatic TBA(P=0.0743)induced by LPS treatment.Pretreatment of ZJ617 before LPS injection induced the production of 5 significant metabolites in the intestinal contents:capric acid,isoleucine 1TMS,glycerol-1-phosphate byproduct,linoleic acid,alanine-alanine(P0.05).Conclusions:These results demonstrated that ZJ617 pretreatment alleviated LPS-induced intestinal tight junction protein destruction,and intestinal and hepatic inflammatory and autophagy signal activation in the piglets.