ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2026
[Niranthin ameliorates Crohn's disease-like colitis in mice via antagonizing intestinal epithelial cell apoptosis and regulating intestinal Th1/Th2 immune homeostasis].
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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Abstract
objectivesTo investigate the effect of niranthin (Nir) in mice with Crohn's disease (CD)‑like colitis and its therapeutic mechanism.
methodsIn a mouse model of CD-like colitis induced using 2,4,6-trinitrobenzene sulfonic acid, the effects of niranthin on colitis symptoms were evaluated by measuring changes in disease activity index (DAI) score, body weight, colon length, and colonic pathologies. Intestinal barrier function and cell apoptosis were evaluated using AB-PAS staining, immunofluorescence staining, Western blotting, and TUNEL staining. The changes in Th1 and Th2 cells in the mesenteric lymph nodes and colonic TNF-α and IL-10 expression levels were determined with flow cytometry and ELISA. In lipopolysaccharide (LPS)-induced mouse colon organoids, the effects of niranthin on organoid budding number and barrier protein expressions were observed. Network pharmacology and
resultsIn the mouse models of CD-like colitis, niranthin treatment obviously improved weight loss, DAI scores, and colorectal shortening and significantly reduced tissue inflammation scores, goblet cell loss, and intestinal epithelial cell apoptosis. Niranthin significantly increased the budding number in LPS-induced mouse colon organoids. In both mouse colon tissues and LPS-induced mouse colon organoids, niranthin obviously increased the expressions of ZO-1 and claudin-1, downregulated the expressions of cleaved caspase-3 and BAX, and upregulated Bcl‑2 expression. The niranthin-treated mouse models showed significantly ameliorated Th1/Th2 imbalance in the mesenteric lymph nodes, downregulated TNF‑α and upregulated IL‑10 levels in the colon tissues. Network pharmacology predicted that the therapeutic mechanism of niranthin for CD-like colitis involved the PI3K/AKT pathway, which was validated in the mouse models treated with niranthin and the PI3K/AKT pathway activator Recilisib.
conclusionsNiranthin ameliorates colitis in mice by antagonizing epithelial apoptosis and regulating Th1/Th2 balance via inhibiting the PI3K/AKT pathway.
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