桃叶珊瑚苷对压力负荷诱导的小鼠心肌纤维化的影响及机制研究

Effect of Aucubin on Myocardial Fibrosis Induced by Pressure Overload in Mice and Its Mechanisms

目的:探讨桃叶珊瑚苷对压力负荷诱导的心肌纤维化的改善作用及其机制。方法:应用随机数字列表法将40只小鼠分为4组:假手术组、假手术+桃叶珊瑚苷组、手术组、手术+桃叶珊瑚苷组,每组10只。采用主动脉缩窄术建立压力负荷诱导的心肌纤维化模型。术后第3天腹腔注射桃叶珊瑚苷(5 mg·kg^-1·d^-1),连续至术后4周。采用CD31免疫组织化学染色检测血管密度,免疫荧光染色检测间质细胞标志物a-平滑肌肌动蛋白(α-SMAA)表达,蛋白免疫印迹法检测内皮细胞标志物CD34、间质细胞标志物α-SMAA和波形蛋白(vimentin)的表达。结果:与假手术组相比,手术组心脏组织中CD31和CD34的表达明显下降,间质细胞标志物α-SMAA和vimentin的表达明显升高(P<0.05)。与手术组相比,经桃叶珊瑚苷处理后,心脏组织中CD31和CD34的表达明显升高,间质细胞标志物α-SMAA和vimentin的表达明显下降(P<0.05)。结论:桃叶珊瑚苷通过抑制内皮间质转化发挥抗心肌纤维化的作用。

Objective:To investigate the effect and mechanism of Aucubin in myocardial fibrosis induced by pressure overload in mice.Methods:Totally 40 mice were divided into 4 groups by the random number list method:the sham operation group,the sham operation+Aucubin group,the operation group,the operation+Aucubin group with 10 ones in each.The pressure overload-induced myocardial fibrosis model was established using aortic binding.Aucubin(5 mg·kg^-1·d^-1)was intraperitoneally injected on the third day after surgery,and continuously treated for 4 weeks.The vascular density was detected by CD31 immunohistochemical staining and the expression of a-smooth muscle actin(α-SMAA)was detected by immunofluorescence staining.The expression of the endothelial cell marker CD34,the interstitial cell markersα-SMAA and vimentin were detected by Western blot.Results:Compared with those in the sham operation group,the expressions of CD31 and CD34 of cardiac tissue in the operation group decreased significantly,and the expressions of interstitial cell markersα-SMAA and vimentin increased significantly(P<0.05).Compared with those in the operation group,the expressions of CD31 and CD34 of cardiac tissue were significantly increased,and the expressions of interstitial cell markersα-SMAA and vimentin significantly decreased after the treatment with Aucubin(P<0.05).Conclusion:Aucubin plays an anti-myocardial fibrosis role via inhibiting endothelial-to-mesenchymal transition.