Evidence map›Paper›PMID 42486818›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2026

[Isovanillic acid alleviates dextran sulfate sodium-induced ulcerative colitis in mice by improving mitochondrial function

Tong Qiao, Longtao Zhang, Yu Zhang, Ju Huang, Qingqing Li, Zhijun Geng, Jianguo Hu, Jing Li

Abstract readEnglish Abstract
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Tong QiaoDepartment of Clinical Laboratory, First Affiliated Hospital of Bengbu Medical University.
Longtao ZhangDepartment of Clinical Laboratory, First Affiliated Hospital of Bengbu Medical University.
Yu ZhangDepartment of Clinical Laboratory, First Affiliated Hospital of Bengbu Medical University.
Ju HuangAnhui Key Laboratory of Basic and Translational Research on Inflammatory Related Diseases, Bengbu 233004, China.
Qingqing LiDepartment of Clinical Laboratory, First Affiliated Hospital of Bengbu Medical University.
Zhijun GengAnhui Key Laboratory of Basic and Translational Research on Inflammatory Related Diseases, Bengbu 233004, China.
Jianguo HuDepartment of Clinical Laboratory, First Affiliated Hospital of Bengbu Medical University.
Jing LiDepartment of Clinical Laboratory, First Affiliated Hospital of Bengbu Medical University.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo investigate the protective effect of isovanillic acid (IVA) against dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice and its underlying mechanism.

methodsForty-eight male C57BL/6 mice were randomly divided into 6 groups (

resultsThe DSS-treated mice showed significantly decreased body weight, increased DAI score, shortened colon length, elevated colonic IL-6 and IL-1β expressions, and severe mucosal damage. IVA, especially at the medium and high doses, obviously improved these changes. Treatment with medium-dose IVA-M significantly increased colonic expressions of ZO-1 and claudin-1, decreased intestinal epithelial cell apoptosis rate and expressions of Bax and cleaved caspase-3, and increased Bcl-2 expression, TOMM20-positive cell counts, and activities of mitochondrial respiratory chain complexes I and IV. In NCM460 cells, IVA treatment obviously reversed DSS-induced mitochondrial impairment, reduced epithelial cell apoptosis, and enhanced expressions of ZO-1 and claudin-1. Network pharmacology analysis suggested that IVA potentially targeted the PPARγ pathway, which was confirmed by increased PPARγ protein expression in IVA-treated mice and NCM460 cells. Treatment with the PPARγ antagonist GW9662 significantly attenuated the protective effect of IVA in DSS-induced NCM460 cells.

conclusionsIVA alleviates DSS-induced colitis in mice by protecting mitochondrial function via activating the PPARγ pathway and suppressing inflammation and apoptosis.

Indexed as

Colitis, UlcerativeMitochondriaPPAR gammaAnimalsApoptosisDextran SulfateDisease Models, AnimalMaleMiceMice, Inbred C57BLSignal TransductionDextran SulfatePPAR gammaPparg protein, mousecell apoptosisintestinal barrierisovanillic acidmitochondrial functionsPPARγ pathwayulcerative colitis

Identifiers

PMID42486818
PMCPMC13391598

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.