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[绿茶多酚通过抑制JAK2/STAT3信号通路对三硝基苯磺酸诱导的小鼠结肠炎肠黏膜屏障功能的保护作用]

[Protective role of green tea polyphenols in intestinal mucosal barrier function of mice with colitis induced by TNBS through inhibiting JAK2/STAT3 pathway].

作者信息

Xi Jin, Ge Sitang, Zuo Lugen, Zhu Yuke, Wang Lian, Xie Qiaoli

机构信息

Anhui Key Laboratory of Tissue Transplantation, Bengbu Medical College Research Center, Bengbu 233030, China.

Department of Gastrointestinal Surgery, First Affiliated Hospital, Bengbu Medical College, Bengbu 233004, China. *Corresponding author, E-mail:

出版信息

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2018 Mar;34(3):237-241.

Abstract

Objective To analyze the therapeutic effect of green tea polyphenols (GTP) in mice with colitis induced by TNBS and its possible mechanism. Methods Colitis was induced by TNBS in BALB/C mice. The mice were randomly divided into GTP group (n=10) and TNBS model group (n=10). Mice in the GTP group were given GTP [0.2 mL at a dose level of 100 mg/(kg.d)] by oral gavage, and mice in the model group were given normal saline [0.2 ml/d] by gavage. Four weeks later, the mice were sacrificed. Disease activity index (DAI) and inflammatory score were evaluated by HE staining. The levels of interleukin 10 (IL-10), IL-6 and tumor necrosis factor α (TNF-α) were detected by ELISA. The expressions and localization of ZO-1 and claudin-1 were identified with immunofluorescence technique. Western blot analysis was performed to detect the expressions of ZO-1, claudin-1, p-JAK2 and p-STAT3 proteins. Results GTP decreased the DAI and inflammatory score, and reduced the levels of TNF-α and IL-6 in TNBS-induced colitis mice at three and four weeks after the administration. Meanwhile, the levels of ZO-1 and claudin-1 increased in the mice of GTP group when compared with those in model group. Western blot analysis showed that GTP down-regulated the JAK2/STAT3 signaling pathway in the intestinal mucosa. Conclusion GTP has a significant therapeutic effect on TNBS-induced colitis through down-regulating the JAK2/STAT3 signaling pathway.

摘要

目的 分析绿茶多酚(GTP)对三硝基苯磺酸(TNBS)诱导的小鼠结肠炎的治疗作用及其可能机制。方法 用TNBS诱导BALB/C小鼠患结肠炎。将小鼠随机分为GTP组(n = 10)和TNBS模型组(n = 10)。GTP组小鼠经口灌胃给予GTP[剂量为100 mg/(kg·d),0.2 mL],模型组小鼠经口灌胃给予生理盐水[0.2 ml/d]。4周后处死小鼠。通过苏木精-伊红(HE)染色评估疾病活动指数(DAI)和炎症评分。采用酶联免疫吸附测定(ELISA)法检测白细胞介素10(IL-10)、IL-6和肿瘤坏死因子α(TNF-α)水平。用免疫荧光技术鉴定紧密连接蛋白1(ZO-1)和闭合蛋白1(claudin-1)的表达及定位。进行蛋白质免疫印迹分析以检测ZO-1、claudin-1、磷酸化JAK2(p-JAK2)和磷酸化信号转导子和转录激活子3(p-STAT3)蛋白的表达。结果 GTP降低了TNBS诱导的结肠炎小鼠给药后3周和4周时的DAI和炎症评分,并降低了TNF-α和IL-6水平。同时,与模型组小鼠相比,GTP组小鼠的ZO-1和claudin-1水平升高。蛋白质免疫印迹分析表明,GTP下调了肠黏膜中的JAK2/STAT3信号通路。结论 GTP通过下调JAK2/STAT3信号通路对TNBS诱导的结肠炎具有显著治疗作用。

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