文献类型：期刊文献

英文题名：Chitosan-gentamicin conjugate attenuates heat stress-induced intestinal barrier injury via the TLR4/STAT6/MYLK signaling pathway: In vitro and in vivo studies

作者：Niu, Xueting[1,2];Hu, Canying[1,2];Chen, Shengwei[1,2];Wen, Jiaying[1,2];Liu, Xiaoxi[1];Yong, Yanhong[1];Yu, Zhichao[1];Ma, Xingbin[1];Li, Chengpeng[3];Warda, Mohamad[4];Abd El-Aty, A. M.[5,6];Gooneratne, Ravi[7];Ju, Xianghong[1,2]

机构：[1]Guangdong Ocean Univ, Coll Coastal Agr Sci, Zhanjiang 524088, Peoples R China;[2]Guangdong Ocean Univ, Shenzheng Inst, Marine Med Res & Dev Ctr, Shenzheng 518120, Peoples R China;[3]Guangdong Ocean Univ, Coll Chem & Environm Sci, Zhanjiang 524088, Peoples R China;[4]Cairo Univ, Fac Vet Med, Dept Biochem & Mol Biol, Giza 12211, Egypt;[5]Cairo Univ, Fac Vet Med, Dept Pharmacol, Giza 12211, Egypt;[6]Ataturk Univ, Med Fac, Dept Med Pharmacol, TR-25240 Erzurum, Turkiye;[7]Lincoln Univ, Fac Agr & Life Sci, Lincoln 7647, New Zealand

年份：2023

卷号：321

外文期刊名：CARBOHYDRATE POLYMERS

收录：SCI-EXPANDED(收录号：WOS:001057260600001)、、EI(收录号：20233314546816)、Scopus(收录号：2-s2.0-85167625339)、WOS

基金：This study was supported by the National Natural Science Founda- tion of China [grant numbers: 31472243, 31902314, 32273077] ; Nat- ural Science Foundation of Guangdong Province, China [grant numbers: 2019A1515011142] ; Innovation Team Project of Department of Edu- cation of Guangdong Province [grant number: 2022KCXTD014] ; Guangdong Postgraduate Education Innovation Project [grant number: 040510052201] ; National Natural Science Foundation of ShenZhen [grant number: JCYJ20220530162008018] and Program for Scientific Research Start -Fund of Guangdong Ocean University [grant number: 101402/R17088] .

语种：英文

外文关键词：Heat stress; CS-GT; Intestinal barrier injury; TLR4/STAT6/MYLK

外文摘要：Heat stress (HS) has a negative impact on animal health. A modified chitosan-gentamicin conjugate (CS-GT) was prepared to investigate its potential protective effects and mechanism of action on heat stress-induced intestinal mucosa injury in IPEC-J2 cells and mouse 3D intestinal organs in a mouse model. CS-GT significantly (P < 0.01) reversed the decline in transmembrane resistance and increased the FITC-dextran permeability of the IPEC-J2 monolayer fusion epithelium caused by heat stress. Heat stress decreased the expression of the tight binding proteins occludin, claudin1, and claudin2. However, pretreatment with CS-GT significantly increased (P < 0.01) the expression of these tight binding proteins. Mechanistically, CS-GT inhibited the activation of the TLR4/ STAT6/MYLK signaling pathway induced by heat stress. Molecular docking showed that CS-GT can bind effectively with TLR4. In conclusion, CS-GT alleviates heat stress-induced intestinal mucosal damage both in vitro and in vivo. This effect is mediated, at least partly, by the inhibition of the TLR4/STAT6/MYLK signaling pathway and upregulation of tight junction proteins. These findings suggest that CS-GT may have therapeutic potential in the prevention and treatment of heat stress-related intestinal injury.