European cytokine network · 2026
Procaine hydrochloride improves DSS-induced colitis via inhibition of IL-6/STAT3 and FOXP3 methylation.
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Xiong An, Tian Yi, Liang Xin, Liu Shaoqun, Shi Chencheng, Cao Yiou, Su Chang
Аннотация
BACKGROUNDS: Disruption 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.
METHODS: Using 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).
RESULTS: Procaine 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.
CONCLUSIONS: The 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.
METHODS: Using 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).
RESULTS: Procaine 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.
CONCLUSIONS: The 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.