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姜黄素通过调节 Treg/Th17 信号通路改善 DSS 诱导的小鼠结肠炎。

Curcumin ameliorates DSS‑induced colitis in mice by regulating the Treg/Th17 signaling pathway.

机构信息

Department of Gastroenterology, Jinan University of Second Clinical Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong 518020, P.R. China.

Department of General Surgery, Shenzhen Children's Hospital, Shenzhen, Guangdong 518026, P.R. China.

出版信息

Mol Med Rep. 2021 Jan;23(1). doi: 10.3892/mmr.2020.11672. Epub 2020 Nov 12.

Abstract

Curcumin has a therapeutic effect on ulcerative colitis, but the underlying mechanism has yet to be elucidated. The aim of the present study was to clarify the possible mechanisms. Dextran sulfate sodium‑induced colitis mice were treated with curcumin via gavage for 7 days. The effects of curcumin on disease activity index (DAI) and pathological changes of colonic tissue in mice were determined. Interleukin (IL)‑6, IL‑10, IL‑17 and IL‑23 expression levels were measured by ELISA. Flow cytometry was used to detect the ratio of mouse spleen regulatory T cells (Treg)/Th17 cells, and western blotting was used to measure the nuclear protein hypoxia inducible factor (HIF)‑1α level. The results demonstrated that curcumin can significantly reduce DAI and spleen index scores and improve mucosal inflammation. Curcumin could also regulate the re‑equilibration of Treg/Th17. IL‑10 level in the colon was significantly increased, while inflammatory cytokines IL‑6, IL‑17 and IL‑23 were significantly reduced following curcumin treatment. No significant difference in HIF‑1α was observed between the colitis and the curcumin group. It was concluded that oral administration of curcumin can effectively treat experimental colitis by regulating the re‑equilibration of Treg/Th17 and that the regulatory mechanism may be closely related to the IL‑23/Th17 pathway. The results of the present study provided molecular insight into the mechanism by which curcumin treats ulcerative colitis.

摘要

姜黄素对溃疡性结肠炎具有治疗作用,但作用机制尚未阐明。本研究旨在阐明其可能的机制。通过灌胃给予葡聚糖硫酸钠诱导的结肠炎小鼠姜黄素 7 天,检测姜黄素对小鼠疾病活动指数(DAI)和结肠组织病理变化的影响。采用酶联免疫吸附试验(ELISA)检测白细胞介素(IL)-6、IL-10、IL-17 和 IL-23 表达水平。采用流式细胞术检测小鼠脾调节性 T 细胞(Treg)/Th17 细胞的比值,采用蛋白质印迹法检测核蛋白缺氧诱导因子(HIF)-1α水平。结果表明,姜黄素可显著降低 DAI 和脾脏指数评分,改善黏膜炎症。姜黄素还可调节 Treg/Th17 的再平衡。姜黄素治疗后结肠中 IL-10 水平显著升高,而炎症细胞因子 IL-6、IL-17 和 IL-23 水平显著降低。结肠炎组和姜黄素组的 HIF-1α 无显著差异。结论:口服姜黄素通过调节 Treg/Th17 的再平衡可有效治疗实验性结肠炎,其调节机制可能与 IL-23/Th17 途径密切相关。本研究结果为姜黄素治疗溃疡性结肠炎的机制提供了分子依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55a4/7684861/69e96bf41ffd/mmr-23-01-11672-g00.jpg

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