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作 者:郑红花[1] 李映红[1] 罗德生[1] 刘琴[2] 屈伸[3]
机构地区:[1]咸宁学院医学院生物化学与分子生物学系,湖北省咸宁市437100 [2]湖北黄石理工学院医学院,湖北省黄石市435000 [3]华中科技大学同济医学院生物化学与分子生物学系,湖北省武汉市430030
出 处:《中国动脉硬化杂志》2006年第4期301-303,共3页Chinese Journal of Arteriosclerosis
基 金:湖北省教育厅重点科研基金资助项目(NO.2003A006)
摘 要:目的探讨川芎嗪对血管紧张素Ⅱ诱导的血管平滑肌细胞增殖的影响。方法建立血管紧张素Ⅱ诱导血管平滑肌细胞增殖模型,用酶促反应定磷法观察不同浓度的川芎嗪在不同时段内对血管平滑肌细胞中钙调蛋白和钙调神经磷酸酶活性的影响。结果与正常对照组比较,血管紧张素Ⅱ组能够明显刺激血管平滑肌细胞增殖,血管紧张素Ⅱ处理的血管平滑肌细胞的钙调蛋白和钙调神经磷酸酶活性及细胞增殖活度均较正常对照组显著增高(P<0.01)。同时加川芎嗪处理后,各组钙调蛋白和钙调神经磷酸酶活性均显著下降(P<0.01)。结论川芎嗪对血管紧张素Ⅱ诱导的血管平滑肌细胞增殖有显著抑制作用,其抑制机制可能与其干预钙调神经磷酸酶依赖的信号转导途径有关。Aim To study the effects of tetramethylpyrazine (TMP) on calmodulin (CAM) and calcinuerin (CAN) in the proliferation of vascular smooth muscle cell(VSMC) induced by angiotensinⅡ ( Ang Ⅱ). Methods A cell proliferating model of VSMC induced by angiotensinⅡ ( Ang Ⅱ) was established; the varity of CaM and CaN activities affected by tetramethylpyrazine (TMP) at different time and different concentration was observed by enzyme reaction phosphorus measurement. Results Cell proliferation activity, CaM and CaN activities were increased significantly in VSMC proliferation induced by Ang Ⅱ(P〈0.01). While treated with TMP, the index were obviously reduced eompared with AngⅡgroup(P〈0.01). Conclusions The VSMC proliferation induced by AngⅡ can be inhibited by TMP significantly, and the inhibiting mechanism of TMP may be related to inhibiting CaM and CaN activities then restraining the proliferation of VSMC in a dose and time-dependent manner.
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