文献类型：期刊文献

英文题名：Tea Tree Oil Terpinen-4-ol Protects Gut Barrier Integrity by Upregulation of Tight Junction Proteins via the ERK1/2-Signaling Pathway

作者：Yong, Yanhong[1,2];Fang, Biao[2];Huang, Yingxin[2];Li, Junyu[3];Yu, Tianyue[3];Wu, Lianyun[3];Hu, Canying[3];Liu, Xiaoxi[1];Yu, Zhichao[2];Ma, Xingbin[2];Gooneratne, Ravi[4];Li, Sidong[5];Abd El-Aty, A. M.[6,7];Ju, Xianghong[1,2]

机构：[1]Guangdong Ocean Univ, Shenzhen Inst, Shenzhen, Peoples R China;[2]Guangdong Ocean Univ, Coll Agr Sci, Dept Vet Med, Zhanjiang, Peoples R China;[3]Guangdong Ocean Univ, Coll Agr Sci, Dept Anim Sci, Zhanjiang, Peoples R China;[4]Lincoln Univ, Fac Agr & Life Sci, Dept Wine Food & Mol Biosci, Lincoln, New Zealand;[5]Guangdong Ocean Univ, Coll Chem & Environm, Zhanjiang, Peoples R China;[6]Cairo Univ, Fac Vet Med, Dept Pharmacol, Giza, Egypt;[7]Ataturk Univ, Med Fac, Dept Med Pharmacol, Erzurum, Turkey

年份：2022

卷号：8

外文期刊名：FRONTIERS IN NUTRITION

收录：SCI-EXPANDED(收录号：WOS:000753707600001)、、Scopus(收录号：2-s2.0-85124533308)、WOS

基金：Funding This study was supported by National Natural Science Foundation of China (Nos. 31472243 and 31902314), Natural Science Foundation of Guangdong Province, China (No. 019A1515011142), and Project of Enhancing School with Innovation of Guangdong Ocean University (No. GDOU230419057).

语种：英文

外文关键词：inflammatory bowel disease; terpinen 4-ol; ERK1; 2-signaling pathway; tight junction (TJ) proteins; mouse model

外文摘要：Tea tree oil (TTO) exhibits a potent antioxidant, antibacterial, and anti-inflammatory activity and is commonly used in skincare products. However, it is not clear whether TTO can protect gut barrier damage in inflammatory bowel disease (IBD) patients. Herein, we report the impact of terpinen-4-ol (TER, the primary constituent of TTO), on lipopolysaccharide (LPS)-induced intestinal epithelial cell barrier function impairment in intestinal porcine epithelial cell lines (IPEC-J2) and dextran sulfate sodium (DSS)-induced IBD in mice. TER protected against LPS-induced damage in IPEC-J2 cells in vitro and attenuated DSS-induced colitis in vivo. Added TER promoted the tight junction (TJ) proteins expressing in vitro and in vivo and attenuated the LPS-induced upregulation of ERK phosphorylation in IPEC-J2 cells. However, when an inhibitor of ERK phosphorylation was added, TER did not promote the expression of TJ protein, denoting that the ERK signaling pathway mediates the upregulation of TJ proteins. Our data may propose the potential application of TER in treating IBD.