Atractylenolide Ⅰ ameliorates post-infectious irritable bowel syndrome by inhibiting the polymerase Ⅰ and transcript release factor and c-Jun N-terminal kinase/inducible nitric oxide synthase pathway  

作　　者：YUAN Jianan CHENG Kunming LI Chao ZHANG Xiang DING Zeyu LI Bing ZHENG Yongqiu 

机构地区：[1]Provincial Engineering Laboratory for Screening and Re-evaluation of Active Compounds of Herbal Medicines in Southern Anhui,Teaching and Research Section of Traditional Chinese Medicine,School of Pharmacy,Wannan Medical College,Wuhu 241000,China [2]Institute of Chinese Materia Medica,China Academy of Chinese Medical Sciences,Beijing 100700,China

出　　处：《Journal of Traditional Chinese Medicine》2025年第1期57-65,共9页中医杂志(英文版)

基　　金：The University Collaborative Innovation Project of Anhui:Creation of a Combined Animal Model of Coronary Heart Disease based on the Theory of Xin'an Medicine(No.GXXT-2020-024);Start-up Funding for Doctoral Research at Wannan Medical College(WYRCQD2018009);Horizontal Project of South Anhui Medical College(H202003)。

摘　　要：OBJECTIVE:To explore the therapeutic effect and target of atractylenolide I(AT-I)on post-infectious irritable bowel syndrome(PI-IBS)rats.METHODS:Therefore,the preliminarily mechanism of AT-I in anti-PI-IBS were first predicted by network pharmacology and molecular docking,then the possible signaling pathways were systematically analyzed.Finally,the potential therapeutic targets and possible signaling pathways of AT-I on PI-IBS in Sprague-Dawley(SD)rat model were verified by experiments.RESULTS:AT-I could alleviate PI-IBS symptoms and reduce the expression of tumor necrosis factorα,interleukin-6 and Interferon-gamma in PI-IBS SD rat model and inhibit the c-Jun N-terminal kinase/inducible nitric oxide synthase(JNK/iNOS)pathway.Notably,AT-I treatment could inhibit the overexpression of polymeraseⅠand transcript release factor(PTRF).CONCLUSION:AT-I could alleviate PI-IBS symptoms through downregulation of PTRF and inhibiting the JNK/iNOS pathway.This study not only provides a scientific basis to clarify the anti-PI-IBS effect of AT-I and its mechanism but also suggests a novel promising therapeutic strategy to treat the PI-IBS.

关 键 词：atractylenolideⅠ post-infectious irritable bowel syndrome polymeraseⅠand transcript release factor network pharmacology MAP kinase signaling system nitric oxide synthase typeⅡ 

分 类 号：R285[医药卫生—中药学]