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| 丹红注射液对心梗大鼠心肌细胞凋亡及JAK2/STAT3信号通路的影响 |
| Effects of Danhong injection on cardiomyocyte apoptosis and JAK2/STAT3 signal pathway in rats with myocardial infarction |
| 投稿时间：2018-08-09 修订日期：2018-08-15 |
| DOI： |
| 中文关键词: 丹红注射液 心肌梗死 细胞凋亡 JAK2/STAT3 |
| 英文关键词: Danhong injection myocardial infarction apoptosis JAK2/STAT3 |
| 基金项目:国家自然科学基金青年项目 |
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| 中文摘要: |
| 目的：研究中药复方制剂丹红注射液对冠脉结扎大鼠心肌细胞凋亡的影响及相关分子机制。方法：取40只雄性Sprague-Dawley（SD）大鼠随机分为假手术组、模型组、丹红注射液低、中、高剂量组，左前降支冠状动脉结扎法造成急性心梗模型，采用超声心动图法记录大鼠心功能，TUNEL标记法检测心肌组织细胞凋亡状况，蛋白免疫印迹法检测心肌组织B细胞淋巴瘤/白血病-2基因（Bcl-2）、Bcl-2相关X蛋白（Bax）的表达、天冬氨酸蛋白水解酶-3（Caspase-3）的活化、Janus激酶2（Janus kinase 2, JAK2）和信号转导及转录激活因子3（signal transducer and activator of transcription 3, STAT3）的磷酸化水平。结果：丹红注射液能剂量依赖性地升高大鼠心功能指标左室射血分数（left ventricular ejection fraction, LVEF）和左室短轴缩短率（left ventricular fractional shortening, LVFS）的值，减少缺血损伤诱导的心肌细胞凋亡，增加抗凋亡基因Bcl-2的表达，减少促凋亡基因Bax的表达及Caspase-3的活化，并上调JAK2和STAT3的磷酸化水平。结论：丹红注射液可显著改善大鼠心功能，抑制缺血诱导的心肌细胞凋亡，其机制可能与调节凋亡相关基因及JAK2/STAT3信号通路参与调控有关。 |
| 英文摘要: |
| Objective: To investigate the effects of Danhong injection (DHI) on cardiomyocyte apoptosis and related molecular mechanisms in rats with myocardial infarction (MI). Methods: 40 male Sprague-Dawley rats were randomly divided into five groups: Sham-operated group; MI + saline group; MI + DHI 0.5mL/kg group; MI + DHI 1mL/kg group; MI + DHI 2mL/kg group, and acute MI were induced by ligation of left anterior descending coronary artery. After intravenous injection for 7 days, the cardiac function of rats was assessed by echocardiography. Then the cardiomyocyte apoptosis index was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) technology, and the expression of B-cell lymphoma/lewkmia-2 (Bcl-2), Bcl-2 associated X protein (Bax), Cleaved cysteine aspartate protease-3 (Caspase-3), and phosphorylation levels of JAK2 and STAT3 in myocardium were determined by western blot analysis. Results: DHI restored cardiac function evidenced by increases of left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) in a dose-dependent manner, and inhibited cardiomyocytes apoptosis induced by ischemia injury. Furthermore, DHI increased Bcl-2 expression, while decreased Bax and active caspase-3 expression. The phosphorylation of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) were also upregulated by DHI. Conclusion: DHI could significantly improve left ventricular function of MI rats, and inhibit ischemia-induced cardiomyocytes apoptosis. These beneficial effects may be associated with the regulation of apoptosis related gene and JAK2/STAT3 signal pathway. |
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