参松养心粉剂对心肌纤维化的改善作用  

Protective Effect of Shensong Yangxin Puvis on Cardiac Fibrosis

作　　者：沈涤非[1] 吴青青[1] 邓伟[1] 倪健[1] 唐其柱[1] SHEN Difei;WU Qingqing;DENG Wei;NI Jian;TANG Qizhu(Department of Cardiology,Renmin Hospital of Wuhan University;Cardiovascular Research Institute,Wuhan University;Hubei Key Laboratory of Cardiology,Wuhan 430060,China)

机构地区：[1]武汉大学人民医院心内科武汉大学心血管病研究所心血管病湖北省重点实验室,武汉430060

出　　处：《医药导报》2018年第9期1051-1055,共5页Herald of Medicine

摘　　要：目的探讨参松养心粉剂对压力负荷诱导的心肌纤维化的改善作用及其机制。方法 C57/BL6小鼠45只,随机分为假手术组、模型对照组和参松养心组(n=15)。采用主动脉结扎建立心肌纤维化模型。采用免疫组织化学方法检测心脏微血管密度(MVD);免疫荧光检测间质标志物α平滑肌肌动蛋白(α-SMA)的表达;免疫荧光染色和蛋白免疫印迹法检测血小板-内皮细胞黏附分子CD31、CD34、α-SMA和波形蛋白的表达变化和内皮间质转化(End MT)的程度。结果参松养心粉剂处理后小鼠血管密度增加(P<0.05);内皮标志物蛋白表达量显著增加,而间质细胞标志物(α-SMA和波形蛋白)的蛋白表达量明显减少(P<0.05)。结论参松养心粉剂可以抑制内皮向间质转化,从而改善压力负荷诱导的心肌纤维化。Objective To investigate the effect of Shensong Yangxin(SSYX)puvis on cardiac fibrosis and the underlying mechanisms.Methods Aortic banding(AB)was performed to induce cardiac fibrosis.Forty-five C57/BL6 mice were randomly assigned into three groups:vehicle sham group,vehicle AB group,and the SSYX AB group(n=15 each gorup).Microvascular density(MVD)was evaluated by immunohistochemistry method.The expression levels of CD31,CD34,αsmooth muscle actin(α-SMA)and vimentin were detected by immunofluorescence staining and western blotting evaluated the extent of endothelial to mesenchymal transition(EndMT).Results The capillary density increased(P<0.05),the protein expression of endothelial markers increased significantly,while the protein expression of interstitial cell markers(alpha-SMA and vimentin)decreased significantly(P<0.05)after SSYX treatment.Conclusion SSYX may attenuate cardiac fibrosis via regulating EndMT which is probably mediated by blockade of TGF-β/Smad pathway.

关 键 词：参松养心粉剂 纤维化 心肌 内皮间质转化 

分 类 号：R286[医药卫生—中药学] R972[医药卫生—中医学]