Procaine hydrochloride improves DSS-induced colitis via inhibition of IL-6/STAT3 and FOXP3 methylation.

An Xiong, Yi Tian, Xin Liang, Shaoqun Liu, Chencheng Shi, Yiou Cao, Chang Su

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Article in European cytokine network, 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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7 authors.

An Xiong *Department of Surgery, Minhang Hospital, Fudan University, Shanghai, China.

Yi Tian *Department of Stomatology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.

Xin LiangShanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai, China.

Shaoqun LiuDepartment of Surgery, Minhang Hospital, Fudan University, Shanghai, China.

Chencheng ShiDepartment of Surgery, Minhang Hospital, Fudan University, Shanghai, China.

Yiou CaoDepartment of Surgery, Minhang Hospital, Fudan University, Shanghai, China.

Chang SuDepartment of Surgery, Minhang Hospital, Fudan University, Shanghai, China.

Funding

Minhang district's medicine, education and research synergistic health service system

6 · The paper itself

Abstract

backgroundsDisruption of immune barrier function is considered a hallmark feature of inflammatory bowel disease. In the present study, the potential effects of the methyltransferase inhibitor procaine hydrochloride on intestinal barrier integrity, as well as T cell differentiation in the context of inflammatory bowel disease were explored.

methodsUsing an experimental model of dextran sulfate sodium-induced ulcerative colitis, mice received daily treatment with either sulfasalazine (100 mg/kg) or procaine hydrochloride (45 mg/kg), or saline (10 μL/g) as a negative control, for 7 consecutive days. Subsequent analysis included disease activity index score, histopathology, expression levels of intestinal epithelial tight junctions and apoptotic protein, production of inflammatory cytokines, frequencies of lymphocyte populations in the spleen by flow cytometry and methylation levels of Forkhead box protein 3 (FOXP3).

resultsProcaine alleviated dextran sulfate sodium-induced colitis, with a reduced disease activity index (p < 0.05) and histopathological score (p < 0.001). Procaine treatment resulted in a 1.96-fold increase in splenic FOXP3+ CD25+ Tregs (p < 0.001). Administration of procaine significantly enhanced tight junction expression (p < 0.01), decreased the expression of BAX and cleaved caspase-3 protein expression, while increasing that of the anti-apoptotic protein BCL-2. Procaine also significantly suppressed IL-6/signal transducer and activator of transcription factor 3 (STAT3) signaling pathway. In addition, procaine amplified FOXP3+ Tregs by inhibiting FOXP3 methylation.

conclusionsThe protective potential of procaine hydrochloride against intestinal barrier injury in colitis may be attributed to increased abundance of Tregs and the augmentation of their anti-inflammatory properties. The potential mechanisms may involve modulation of IL-6/STAT3 signaling pathway and inhibition of FOXP3 methylation.

Indexed as

ColitisForkhead Transcription FactorsInterleukin-6STAT3 Transcription FactorAnimalsColitis, UlcerativeDextran SulfateDisease Models, AnimalIntestinal MucosaMaleMethylationMiceSignal TransductionDextran SulfateForkhead Transcription FactorsFoxp3 protein, mouseInterleukin-6Stat3 protein, mouseSTAT3 Transcription Factorforkhead box protein 3interleukin-6/signal transducer and activator of transcription factor 3 signaling pathwayintestinal mucosal barrierprocaine hydrochlorideTregsUlcerative colitis

Identifiers

PMID42421502

DOI10.1016/j.pharmthera.2025.108831

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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.