强心方组分对心肌梗死后心力衰竭小鼠心功能的影响

目的 研究强心方中三味主药黄芪、附子、葶苈子单独使用与联合使用对心肌梗死后心力衰竭心脏的保护作用。 方法 构建小鼠急性心肌梗死模型,模型建立第2天开始经食道给予药物治疗,分为假手术组(Sham)、手术对照组(PBS)、黄芪总提取物单独给药组(HQ)、附子总提取物单独给药组(FZ)、葶苈子总提取物单独给药组(TLZ)、1/3剂量混合给药组(黄芪总提取物+附子总提取物+葶苈子总提取物,Mix)、全剂量混合给药组(黄芪总提取物+附子总提取物+葶苈子总提取物,Mix full-dose)。给药30d后观察各组分对心肌梗死后小鼠心功能的影响。 结果 给药30d后心脏超声结果显示,各给药组小鼠的心脏功能相对于PBS组则均有不同程度的改善(P<0.05)。心肌组织切片染色结果显示各给药组小鼠的心肌梗死面积与PBS组相比均有显著的减少,心室重构程度显著减轻(P<0.05)。免疫荧光染色结果显示给药组小鼠心肌细胞增生肥大程度降低(P<0.05)。 结论 黄芪、附子、葶苈子联合使用可以显著提高心肌梗死后小鼠的心功能,改善小鼠的左室重构,减轻心肌组织纤维化以及心肌细胞肥大,并促进心肌梗死后血管新生。尤其是1/3剂量混合治疗组好于全剂量混合治疗组,这些结果对于中药临床上剂量的应用具有明显的指导作用。
Objective To investigate the protective effect of the main components of Chinese medicine Qiangxin decoction astragalus membranaceus, aconite and semen lepidii on heart function in mice with myocardial infarction. Methods The acute myocardial infarction model was established in mice and the sham operation was performed in sham group. After AMI was induced, the mice were administrated by gavage with PBS (Sham group), Astragalus (HQ group), Aconite (FZ group), Semen lepidii (TLZ group), 1/3 dose of mix components (Mix group) and whole dose mixed components (Mix-full group). After 30 days of administration, the effects on cardiac function in various groups were observed and compared. Results After 30 days of administration,cardiac ultrasonography result showed that the cardiac function of the mice in administration groups was improved (P<0.05). The results of Immunohistochemistry showed that the myocardial infarct size in administration groups was significantly decreased, and the degree of ventricular remodeling was significantly ameliorated (P<0.05). Immunofluorescence staining showed that the hypertrophy was ameliorated (P<0.05). The cardiac protect effect of 1/3 dose mixed administration group was better than that of whole dose mixed administration group. Conclusion The main components of Qiangxin Decoction Astragalus membranaceus, Aconite and Semen lepidii significantly can improve the cardiac function, improve left ventricular remodeling and reduce myocardial fibrosis and myocardial hypertrophy after myocardial infarction in mice