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 

作者机构：Provincial Engineering Laboratory for Screening and Re-evaluation of Active Compounds of Herbal Medicines in Southern AnhuiTeaching and Research Section of Traditional Chinese MedicineSchool of PharmacyWannan Medical College Institute of Chinese Materia MedicaChina Academy of Chinese Medical Sciences 

出 版 物：《Journal of Traditional Chinese Medicine》 (中医杂志(英文版))

年 卷 期：2025年第45卷第1期

页      面：57-65页

核心收录：

学科分类：1008[医学-中药学(可授医学、理学学位)] 1006[医学-中西医结合] 100602[医学-中西医结合临床] 10[医学] 

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) 

主　　题：MAP kinase signaling system atractylenolide Ⅰ network pharmacology nitric oxide synthase type Ⅱ polymerase Ⅰ and transcript release factor post-infectious irritable bowel syndrome 

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 factor α, 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 polymerase Ⅰ and 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.