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 a,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-Ⅰtreatment 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.