姜黄素抑制哮喘大鼠气道平滑肌细胞TGFβ1表达探究.docVIP

姜黄素抑制哮喘大鼠气道平滑肌细胞TGFβ1表达探究.doc

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姜黄素抑制哮喘大鼠气道平滑肌细胞TGFβ1表达探究

姜黄素抑制哮喘大鼠气道平滑肌细胞TGFβ1表达探究   [摘要] 目的 观察姜黄素对哮喘大鼠气道平滑肌细胞(ASMC)增殖及TGFbeta;1表达的影响。 方法 将24只雄性SD大鼠分为对照组、哮喘组和姜黄素组。以卵清白蛋白(OVA)致敏激发建立哮喘大鼠气道重塑模型,图像分析技术测定支气管壁厚度(Wat)和平滑肌厚度(Wam),免疫组织化学法(IHC)测定肺组织 TGFbeta;1 蛋白表达。酶联免疫吸附法(ELISA)测定细胞培养液中TGFbeta;1含量,实时定量 PCR(Real-time PCR)检测ASMC中TGFbeta;1mRNA表达,CCK-8分析ASMC增殖程度。 结果 姜黄素组与哮喘组相比,Wat及Wam厚度减少(Plt;0.01),仍高于对照组(Plt;0.01);IHC显示:姜黄素组肺组织中 TGFbeta;1蛋白表达与哮喘组比较明显减少(Plt;0.01),仍高于对照组(Plt;0.01)。姜黄素组大鼠ASMC中TGFbeta;1和TGFbeta;1mRNA表达均降低,与对照组比较差异有统计学意义(Plt;0.01);姜黄素组ASMC增殖明显受到抑制(Plt;0.01)。 结论 姜黄素能抑制哮喘大鼠ASMC增殖,其机制与降低TGFbeta;1的表达有关。  [关键词] 转化生长因子beta;1;大鼠;哮喘;气道重塑;姜黄素  [中图分类号] R285.5 [文献标识码] A [文章编号] 1673-9701(2016)19-0034-04  [Abstract] Objective To study the role of curcumin on proliferation mechanism of airway smooth musle cell (ASMC) and TGFbeta;1 expression in asthmatic rats. Methods A total of 24 Sprague-Dawley(SD) rats were sensitized and challenged by OVA to establish asthmatic model were divided into three groups with 8 rats in each group. The total bronchial wall thickness(Wat) and the airway smooth musle thickness(Wam) were measured by image analysis system. The TGFbeta;1 expressions were determined by immunohistochemistry. Vitro experiments were conducted to determine the direct effect of curcumin on TGFbeta;1 expression by ASMC. Real-time PCR was employed to detect the expression of TGFbeta;1 mRNA levels. TGFbeta;1 concentrations were determined by sandwich enzyme-linked immunosorbent assay(ELISA). Cell Counting Kit-8(CCK-8) was used to detect ASMC proliferation. Results Wat and Wam of curcumin group were significantly thiner than asthma group (Plt;0.01); but those were significantly thicker than control group (Plt;0.01). The TGFbeta;1 expressions in the curcumin group was significantly lower than those of the asthmatic group(Plt;0.01); but they were higher than the control group (Plt;0.01). Compared to control group, curcumin decreased the protein expressions and mRNA expressions of TGFbeta;1 of ASMC (Plt;0.01), inhibited ASMC proliferation (P

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