ArticleJournal of traditional Chinese medicine = Chung i tsa chih ying wen pan2025
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.
Article in Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Pinggan Yuyin Qingre formula ameliorates meibomian gland dysfunction through the interleukin-17/nuclear factor kappa B pathway based on network pharmacology and experimental validation.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- The interplay between recovery and immunity in infectious and non-communicable diseases.Frontiers in cellular and infection microbiology · 2026Review
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7 authors.
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Abstract
objectiveTo explore the therapeutic effect and target of atractylenolide I (AT-I) on post-infectious irritable bowel syndrome (PI-IBS) rats.
methodsTherefore, 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.
resultsAT-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).
conclusionAT-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.
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