摘要
目的观察黄芩苷灌胃对病毒性心肌炎小鼠心肌细胞凋亡的影响,并探讨其机制。方法 60只Balb/c小鼠,随机分为对照组,病毒性心肌炎组,黄芩苷低、中、高剂量组及黄芪总黄酮组,各10只。后五组制备病毒性心肌炎模型,黄芩苷低、中、高剂量组在此基础上分别给予黄芩苷20、50、100 mg/(kg·d)灌胃,黄芪总黄酮组在此基础上给予黄芪总黄酮0.35 mg/(kg·d)腹腔注射,对照组仅给予等体积0.9%NaCl溶液腹腔注射,1次/d,连续10 d。采用超声心动图检测各组小鼠心功能指标;采用酶联免疫吸附法检测血清氨基末端脑钠肽前体(NT-proBNP)水平;采用流式细胞仪观察心室肌细胞凋亡以及细胞线粒体膜电位变化情况;采用Western blotting法检测心室肌细胞中Cyt C、Caspase-9、Caspase-3表达情况;采用Caspase-9、Caspase-3活性检测试剂盒观察心室肌细胞Caspase-9、Caspase-3活化情况。结果与对照组比较,病毒性心肌炎组小鼠心功能下降,血清NT-proBNP水平升高,心肌细胞凋亡率升高,心室肌细胞线粒体膜电位降低,心室肌细胞Cyt C、Caspase-9、Caspase-3表达升高,心室肌细胞Caspase-3、Caspase-9活性增强(P均<0.05)。与病毒性心肌炎组比较,黄芩苷低、中、高剂量组及黄芪总黄酮组小鼠心功能好转,血清NT-proBNP水平降低,心肌细胞凋亡率下降,心室肌细胞线粒体膜电位升高,心室肌细胞中Cyt C、Caspase-9、Caspase-3表达降低,心室肌细胞Caspase-3、Caspase-9活性减弱(P均<0.05)。结论黄芩苷灌胃可抑制病毒性心肌炎小鼠心肌细胞凋亡,其机制可能与升高病毒性心肌炎小鼠心肌细胞线粒体膜电位,缓解线粒体损伤,抑制Cyt C/Caspase-9/Caspase-3凋亡信号通路表达与活化有关。
Objective To observe the effect of intragastric administration of baicalin on cardiomyocyte apoptosis in mice with viral myocarditis and to explore its mechanism. Methods Sixty Balb/c mice were randomly divided into the control group, viral myocarditis group, low-dose, medium-dose, and high-dose baicalin groups, and astragalus flavonoids group, with 10 in each. Viral myocarditis models were prepared in the latter five groups. Baicalin was given to mice in the low-dose, medium-dose, and high-dose baicalin groups by intragastric administration of 20, 50, and 100 mg/(kg·d) baicalin, respectively. Mice in the astragalus flavonoids group were given 0.35 mg/(kg·d) astragalus flavonoids on this basis. The mice in the control group was given the same volume of 0.9% NaCl solution, once a day, for 10 days. Cardiac function was measured by echocardiography, the serum level of NT-proBNP was measured by enzyme-linked immunosorbent assay, and the apoptosis of ventricular myocytes and changes of mitochondrial membrane potential were observed by flow cytometry. The expression levels of Cyt C, Caspase-9 and Caspase-3 in the ventricular myocytes were detected by Western blotting. Caspase-9 and Caspase-3 activity detection kits were used to observe the activation of Caspase-9 and Caspase-3 in the ventricular myocytes. Results Compared with the control group, the cardiac function of mice in the viral myocarditis group decreased, the serum NT-proBNP level increased, the apoptotic rate of myocardial cells increased, the mitochondrial membrane potential of ventricular myocytes decreased, the expression levels of Cyt C, Caspase-9, and Caspase-3 in the ventricular myocytes increased, and the activity of Caspase-3 and Caspase-9 in the ventricular myocytes increased (all P <0.05). Compared with the viral myocarditis group, the heart function of mice in the low-dose, medium-dose, and high-dose baicalin groups and astragalus flavonoids group was improved, the serum NT-proBNP level decreased, myocardial apoptosis rate decreased, mitochondrial membrane potential of ventricular myocytes increased, the expression of Cyt C, Caspase-9, and Caspase-3 in the ventricular myocytes decreased, and the activity of Caspase-3 and Caspase-9 in the ventricular myocytes decreased (all P <0.05). Conclusions Baicalin can inhibit the cardiomyocyte apoptosis in mice with viral myocarditis by increasing mitochondrial membrane potential, alleviating mitochondrial damage, and inhibiting the expression and activation of apoptotic signal pathway of Cyt C/Caspase-9/Caspase-3.
作者
欧红令
林亚发
林小亮
OU Hongling;LIN Yafa;LIN Xiaoliang(Haikou Fourth People's Hospital, Haikou 571100, China)
出处
《山东医药》
CAS
2019年第7期48-51,共4页
Shandong Medical Journal
关键词
黄芩苷
病毒性心肌炎
心室重构
细胞凋亡
线粒体凋亡信号通路
baicalin
viral myocarditis
ventricular remodeling
apoptosis
mitochondrial apoptosis signaling pathway
