{"title":"Aloe-emodin regulates colon epithelial cell function by regulating HIF-1α to alleviate irritable bowel syndrome.","authors":"Qinghua Wang, Shiyu Lu, Zhonghao Yin","doi":"10.1080/00498254.2025.2559959","DOIUrl":null,"url":null,"abstract":"<p><p>This study aimed to investigate the therapeutic potential of Aloe-emodin (AE) for irritable bowel syndrome (IBS), focusing on its effects and underlying mechanisms.Deoxycholic acid (DCA)-induced IBS rats (Sprague-Dawley) were orally administered AE. Body weight and faecal pellet were monitored. Anxiety-like behaviour, visceral hypersensitivity, colon permeability were assessed <i>via</i> the open-field (OF) test, abdominal Withdrawal Reflex (AWR) score, FITC-dextran fluorescence, respectively. Enzyme-linked immunosorbent assay (ELISA) quantified substance P (SP), 5-hydroxytryptamine (5-HT), TNF-α, and IL-6 levels. Hypoxia inducible factor-1α (HIF-1α) expression was analysed <i>via</i> qRT-PCR. The mechanism of AE on IBS was evaluated in LPS-treated NCM460 injury.AE alleviated IBS symptoms (improved weight gain, reduced faecal output/water content, increased centre exploration time, lowered AWR scores, decreased colon permeability, SP, 5-HT, and pro-inflammatory cytokine levels). HIF-1α upregulation in colonic tissues and LPS-induced NCM460 cells was suppressed by AE treatment. The protective effect of AE was reversed by HIF-1α overexpression in IBS rats. AE enhanced cell proliferation, reduced cellular permeability, and inflammation in LPS-stimulated NCM460 cells. HIF-1α overexpression partially reversed the protective effects of AE in LPS-induced NCM460 injury.AE ameliorated IBS symptoms by promoting cell proliferation, suppressing cell permeability, and inflammation of colonic epithelial cells <i>via</i> regulating HIF-1α.</p>","PeriodicalId":23812,"journal":{"name":"Xenobiotica","volume":" ","pages":"1-11"},"PeriodicalIF":1.2000,"publicationDate":"2025-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Xenobiotica","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/00498254.2025.2559959","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}
引用次数: 0
Abstract
This study aimed to investigate the therapeutic potential of Aloe-emodin (AE) for irritable bowel syndrome (IBS), focusing on its effects and underlying mechanisms.Deoxycholic acid (DCA)-induced IBS rats (Sprague-Dawley) were orally administered AE. Body weight and faecal pellet were monitored. Anxiety-like behaviour, visceral hypersensitivity, colon permeability were assessed via the open-field (OF) test, abdominal Withdrawal Reflex (AWR) score, FITC-dextran fluorescence, respectively. Enzyme-linked immunosorbent assay (ELISA) quantified substance P (SP), 5-hydroxytryptamine (5-HT), TNF-α, and IL-6 levels. Hypoxia inducible factor-1α (HIF-1α) expression was analysed via qRT-PCR. The mechanism of AE on IBS was evaluated in LPS-treated NCM460 injury.AE alleviated IBS symptoms (improved weight gain, reduced faecal output/water content, increased centre exploration time, lowered AWR scores, decreased colon permeability, SP, 5-HT, and pro-inflammatory cytokine levels). HIF-1α upregulation in colonic tissues and LPS-induced NCM460 cells was suppressed by AE treatment. The protective effect of AE was reversed by HIF-1α overexpression in IBS rats. AE enhanced cell proliferation, reduced cellular permeability, and inflammation in LPS-stimulated NCM460 cells. HIF-1α overexpression partially reversed the protective effects of AE in LPS-induced NCM460 injury.AE ameliorated IBS symptoms by promoting cell proliferation, suppressing cell permeability, and inflammation of colonic epithelial cells via regulating HIF-1α.
期刊介绍：
Xenobiotica covers seven main areas, including:General Xenobiochemistry, including in vitro studies concerned with the metabolism, disposition and excretion of drugs, and other xenobiotics, as well as the structure, function and regulation of associated enzymesClinical Pharmacokinetics and Metabolism, covering the pharmacokinetics and absorption, distribution, metabolism and excretion of drugs and other xenobiotics in manAnimal Pharmacokinetics and Metabolism, covering the pharmacokinetics, and absorption, distribution, metabolism and excretion of drugs and other xenobiotics in animalsPharmacogenetics, defined as the identification and functional characterisation of polymorphic genes that encode xenobiotic metabolising enzymes and transporters that may result in altered enzymatic, cellular and clinical responses to xenobioticsMolecular Toxicology, concerning the mechanisms of toxicity and the study of toxicology of xenobiotics at the molecular levelXenobiotic Transporters, concerned with all aspects of the carrier proteins involved in the movement of xenobiotics into and out of cells, and their impact on pharmacokinetic behaviour in animals and manTopics in Xenobiochemistry, in the form of reviews and commentaries are primarily intended to be a critical analysis of the issue, wherein the author offers opinions on the relevance of data or of a particular experimental approach or methodology
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