红景天苷对急性心肌缺血大鼠心肌细胞凋亡的作用及机制研究
| 作者: |
1李杰,
2李俊锋,
1魏婷婷,
1李军华
1 中山大学孙逸仙纪念医院麻醉科，广州 510120 2 广州市增城区人民医院麻醉科，广州 511300 |
| 通讯: |
李杰
Email: medlijie@163.com |
| DOI: | 10.3978/j.issn.2095-6959.2016.07.001 |
| 基金: | 广东省自然科学基金, S2013010014514 广东省教育部产学研结合项目基金, 2012B091100454 中央高校基本科研业务费专项基金, 12ykpy26 |
摘要
目的：观察红景天苷对急性心肌缺血大鼠心肌细胞凋亡的影响，探讨其可能的分子机制。方法：制备Sprague Dawley大鼠急性心肌缺血模型，随机分为红景天苷高、低剂量组(40 mg/kg、10 mg/kg)、急性心肌缺血组和对照组。原位末端转移酶标记染色法检测心肌组织凋亡情况，免疫印迹法检测心肌组织Bcl-2、Bax、Cytochrome c (Cyt-c)、cleaved caspase-3以及cleaved caspase-9蛋白的表达水平。结果：原位末端转移酶标记染色法显示红景天苷浓度依赖性抑制急性心肌缺血所引起心肌细胞的凋亡；免疫印迹法结果显示，与急性心肌缺血组相比，红景天苷干预后心肌组织中Bcl-2的蛋白表达显著增加，Bax的蛋白表达显著减少，胞浆(cyto)中Cyt-c的蛋白表达水平显著下降，cleaved caspase-3和cleaved caspase-9表达均显著降低。结论：红景天苷具有抗心肌细胞凋亡的作用，其作用机制可能是通过抑制线粒体通路减少细胞的凋亡。本实验为红景天苷可作为临床上治疗缺血性心脏病提供实验依据。
关键词：
红景天苷
急性心肌缺血
心肌细胞
凋亡
线粒体
Salidroside inhibits myocardial cell apoptosis in acute myocardial ischemia rats
CorrespondingAuthor: LI Jie Email: medlijie@163.com
DOI: 10.3978/j.issn.2095-6959.2016.07.001
Abstract
Objective: To investigate the effects and mechanisms of salidroside on the myocardial cell apoptosis in acute myocardial ischemia (AMI) rats. Methods: AMI experimental model was established in Sprague Dawley rats, and rats were randomly divided into 4 groups: control, AMI, AMI rats treated with different dose of Salidroside (40 mg/kg, 10 mg/kg). Terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) staining was applied to analyze the myocardial cell apoptosis. The protein expression of Bcl-2, Bax, Cytochrome c (Cyt-c), cleaved caspase-3 and cleaved caspase-9 were determined by Western blot, respectively. Results: Salidroside inhibited AMI-induced myocardial cell apoptosis dose-dependently. Moreover, compared with AMI group, salidroside treatment decreased the expression of Bax, cleaved caspase-3 and cleaved caspase-9 does-dependently. However, the expression of Bcl-2 and the content of mitochondrial Cyt-c were decreased. Conclusion: Salidroside inhibits myocardial cell apoptosis during AMI may be through inactivation of Mitochondria-dependent pathway.