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.

ABSTRACT:

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 co

SUBMITTER: Jianan Y 

PROVIDER: S-EPMC11764933 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature