| 田香,邓德传,兰运辉,等.异丙酚预处理通过上调 Caveolin?3增加缺血心肌细胞线粒体膜稳定性的机制研究[J].安徽医药,2020,24(11):2142-2145. |
| 异丙酚预处理通过上调 Caveolin?3增加缺血心肌细胞线粒体膜稳定性的机制研究 |
| Propofol increases mitochondrial membrane stability， decreases apoptosis and cytochrome C release in rats with myocardial ischemia by up?regulating Caveolin?3 |
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| DOI：10.3969/j.issn.1009?6469.2020.11.006 |
| 中文关键词: 二异丙酚 心肌再灌注 小窝蛋白 ?3 心肌缺血 线粒体膜 细胞色素 C 大鼠， Sprague?Dawley |
| 英文关键词: Propofol Myocardial reperfusion Caveolin?3 Myocardial ischemia Mitochondrial membrane Cytochrome |
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| 中文摘要: |
| 目的探讨异丙酚通过上调小窝蛋白 ?3(Caveolin?3)增加缺血心肌线粒体膜稳定性的机制。方法筛选健康 SD大鼠 36只，体质量范围为 250~300 g，采用随机数字表法分为 3组，每组 12只。 ①正常心肌细胞组:仅开胸不结扎； ②心肌缺血再灌注组:单纯给予以 5％葡萄糖稀释的脂肪乳，持续静脉滴注； ③缺血心肌细胞 +异丙酚预处理组:缺血前 10 min开始持续静脉滴注异丙酚 12 mg·kg-1·h-1，异丙酚用 5％葡萄糖稀释。通过蛋白质免疫印迹检测 Caveolin?3和细胞色素 C；通过荧光探针 DCFH? DA测定 ROS产生；通过阳离子染料 JC?1评估线粒体膜电位； caspase?3比色测定试剂盒测定心肌细胞 caspase?3活性。结果心肌缺血再灌注组 Caveolin?3蛋白活性(0.57±0.09)低于正常心肌细胞组(2.24±0.25)和缺血心肌细胞 +异丙酚预处理组(2.02±0.14)异丙酚改善心肌缺血诱导的 Caveolin?3下调(P＜0.05)；心肌缺血再灌注组 DCF荧光强度(2.79±0.21)高于正常心肌细胞±0.12)缺血心肌细胞 +异丙酚预处理组心肌细胞 DCF荧光强度(1.23±0.14)低于心肌缺血再灌注组(P＜0.05)；与正常心肌细胞组(1±0.06)相比，经受心肌缺血的心肌细胞显示出线粒体去极化降低(0.13±0.02)，缺血心肌细胞 +异丙酚预处理组(1.00，.00，组(0.83±0.11)稳定了线粒体膜电位(P＜0.05)。正常心肌细胞组线粒体细胞色素 C为(1.00±0.08)，心肌缺血再灌注组为(2.76±0.24)，心肌缺血增加线粒体细胞色素 C释放到胞质溶胶中，缺血心肌细胞 +异丙酚预处理组(1.37±0.18)降低细胞色素 C释放(P＜0.05)；心肌缺血再灌注组显示出 caspase?3和 caspase?9活性增加。与心肌缺血再灌注组相比，异丙酚降低了 caspase? 3和 caspase?9活性(P＜0.05)。结论异丙酚在心肌缺血下的保护作用取决于 Caveolin?3的上调，后者降低活性氧产生、增加线粒体膜电位、减少细胞凋亡和细胞色素 C释放。 |
| 英文摘要: |
| Objective This study was designed to investigate whether propofol reduces mitochondrial membrane stability in pa?tients with myocardial ischemia by up?regulating Caveolin?3.Methods 36 healthy SD rats，weighing 250 to 300 g，were screened by the laboratory animal center of the academy of military medical sciences.36 rats were randomly divided into 3 groups with 12rats in each group.(1)Normal myocardial cell group:only thoracotomy without ligation；(2)Ischemic myocardial cell group:in the experiment，fat milk diluted with 5% glucose was given，and continuous intravenous drip was given.(3)Ischemic myocardial cells + propofol treatment group:During the experiment，continuous intravenous infusion of propofol 12 mg·kg-1·h-1 was started 10 min be? fore ischemia，and propofol was diluted with 5% glucose.Waveolin?3 and cytochrome c were detected by Western blotting；fluores? cent probe DCFH?DA was used.ROS production was measured；mitochondrial membrane potential was evaluated by cationic dye JC? 1；caspase?3 activity was measured by caspase?3 colorimetric assay kit.Results Caveolin?3 protein was decreased in myocardial ischemia group，propofol improved Caveolin?3 induced by myocardial ischemia［(2.24±0.25)vs.(0.57±0.09)，(2.02±0.14)，P＜0.05］， DCF fluorescence increased in myocardial ischemia，and DCF fluorescence decreased in propofol group［(2.79±0.21)vs.(1.00±0.12)，(1.23±0.14)，P＜0.05］； Compared with the control，cardiomyocytes subjected to myocardial ischemia showed a de? crease in mitochondrial depolarization，and the propofol group stabilized mitochondrial membrane potential［(1.00±0.06)vs.(0.13±0.02)，(0.83±0.11)，P＜0.05］.Myocardial ischemia increased mitochondrial cytochrome C release into the cytosol，propofol group de? creased cytochrome C release［(1.00±0.08)vs.(2.76±0.24)，(1.37±0.18)，P＜0.05］； myocardial ischemia group showed increasedcaspase?3 and caspase?9 activity.Propofol reduced caspase?3 and caspase?9 activity compared with myocardial ischemia(P＜0.05). Conclusion The protective effect of propofol under myocardial ischemia depends on the upregulation of Caveolin?3，which reduces the production of reactive oxygen species，increases mitochondrial membrane potential，and reduces cytochrome c and apoptosis. |
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