乌头碱对培养新生大鼠心室肌细胞Connexin43蛋白磷酸化的影响

发布时间：2019-07-17 08:12

【摘要】：目的建立细胞水平的染毒模型,观察乌头碱对心肌细胞缝隙连接蛋白Connexin43(Cx43)的影响。方法实验分0.25、0.5、0.75、1.0、1.5和2.0μmol/L等6个不同浓度乌头碱染毒组,运用蛋白印迹法和免疫荧光技术,检测各组及对照组心肌细胞Cx43蛋白磷酸化状态的改变。结果蛋白印迹检测显示,不同浓度染毒组心肌细胞中Cx43蛋白总量与正常对照组无显著差异;0.5μmol/L乌头碱染毒后,Cx43开始出现脱磷酸化;当染毒浓度达到1.0μmol/L后,Cx43脱磷酸化显著,且1.5及2.0μmol/L染毒效果和1.0μmol/L染毒组相当。免疫荧光分析结果提示乌头碱作用后,心肌细胞Cx43蛋白在羧基端第368位点丝氨酸残基(Ser368)发生明显的脱磷酸化。结论一定浓度的乌头碱能诱导心肌细胞缝隙连接蛋白Cx43发生显著脱磷酸化。
[Abstract]:Objective to establish a cell level model and observe the effect of aconitine on gap junction protein Connexin43 (Cx43) in cardiomyocytes. Methods six different concentrations of aconitine exposure groups, 0.25, 0.5, 0.75, 1.0, 1.5 and 2.0 渭 mol / L, were used to detect the phosphorylation of Cx43 protein in cardiomyocytes of each group and control group. Results Western imprinting showed that the total amount of Cx43 protein in cardiomyocytes in different concentrations of aconitine exposure group was not significantly different from that in normal control group. After 0.5 渭 mol / L aconitine exposure, Cx43 began to dephosphorylation, and when the concentration reached 1.0 渭 mol / L, Cx43 dephosphorization and acidizing was significant, and the effect of 1.5 渭 mol / L and 2.0 渭 mol / L exposure was the same as that of 1.0 渭 mol / L aconitine group. The results of immunofluorescence analysis suggested that the dephosphorylation of Cx43 protein at position 368 (Ser368) of cardiomyocytes was observed after aconitine treatment. Conclusion A certain concentration of aconitine can induce significant dephosphorylation of gap junction protein Cx43 in cardiomyocytes.
【作者单位】：华中科技大学同济医学院法医学系湖北省中山医院病理科湖北省中山医院病理科华中科技大学同济医学院法医学系华中科技大学同济医学院法医学系华中科技大学同济医学院法医学系
【分类号】：D919

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