| 赵 灿,王永亮,沈絮华,吴永全,彭 晖.瑞舒伐他汀预处理对心肌缺血再灌注损伤大鼠自噬和凋亡的影响及机制研究[J].现代生物医学进展英文版,2021,(5):806-810. |
| 瑞舒伐他汀预处理对心肌缺血再灌注损伤大鼠自噬和凋亡的影响及机制研究 |
| Study on the Effect and Mechanism of Rosuvastatin Preconditioning on Autophagy and Apoptosis in Rats with Myocardial Ischemia-reperfusion Injury |
| Received:July 28, 2020 Revised:August 24, 2020 |
| DOI：10.13241/j.cnki.pmb.2021.05.002 |
| 中文关键词: 心肌缺血再灌注 瑞舒伐他汀 自噬因子 凋亡 作用机制 |
| 英文关键词: Myocardial ischemia reperfusion Rosuvastatin Autophagy factor Apoptosis Mechanism of action |
| 基金项目:国家自然科学基金项目(81570220) |
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| 中文摘要: |
| 摘要 目的：探讨瑞舒伐他汀预处理对心肌缺血再灌注损伤（MIRI）大鼠自噬因子和凋亡相关基因的影响及作用机制。方法：将60只SD级大鼠纳入研究，遵循随机数字表法分成假手术组、模型组以及预处理组，每组20只。模型组以及预处理组大鼠均制备MIRI模型，假手术组按照相同的方式开胸，仅穿线不进行冠状动脉的结扎。模型制备前7d，预处理组予以瑞舒伐他汀20 mg/（kg?d）灌胃处理，假手术组以及模型组大鼠则予以生理盐水5 mL/d处理。比较三组大鼠心肌组织凋亡率、心肌梗死面积、左心室血流动力学参数、自噬因子P62、Beclin-1蛋白表达水平以及凋亡相关基因Bcl-2、Bax 、CytC蛋白表达水平。结果：预处理组及模型组大鼠的心肌组织凋亡率以及心肌梗死面积均高于假手术组，但预处理组低于模型组（均P＜0.05）。预处理组及模型组大鼠的左心室舒张末压（LVEDP）均高于假手术组，但预处理组低于模型组（均P＜0.05）；预处理组及模型组大鼠的左心室内压最大上升速率（+dp/dtmax）、左心室内压最大下降速率（-dp/dtmax）低于假手术组，但预处理组高于模型组（均P＜0.05）。预处理组及模型组大鼠的P62、Beclin-1蛋白表达水平均高于假手术组，但预处理组低于模型组（均P＜0.05）。预处理组及模型组大鼠Bcl-2 mRNA表达水平低于假手术组，但预处理组高于模型组（均P＜0.05）；预处理组及模型组大鼠Bax mRNA表达水平及CytC蛋白表达水平高于假手术组，但预处理组低于模型组（均P＜0.05）。结论：瑞舒伐他汀预处理可显著减轻MIRI大鼠心肌组织受损程度，其主要作用机制可能与瑞舒伐他汀有效抑制心肌细胞自噬因子表达以及调控凋亡相关基因表达有关。 |
| 英文摘要: |
| ABSTRACT Objective: To study the effects of rosuvastatin preconditioning on autophagy factors and apoptosis-related genes in myocardial ischemia reperfusion injury (MIRI) rats and to analyze their mechanisms. Methods: 60 SD rats were included in the study, and they were randomly divided into sham operation group, model group and pretreatment group, with 20 rats in each group. MIRI models were prepared in both the model group and the pretreatment group. In the sham operation group, thoracotomy was performed in the same way, but only threading was performed without coronary artery ligation. 7d before the model preparation, the pretreatment group was treated with rosuvastatin 20 mg/(kg?d) by gavage, while the sham operation group and the model group were treated with normal saline 5ml/d. Three groups of rats myocardial tissue apoptosis rate and the myocardial infarction area, left ventricular hemodynamic parameters, the expression of P62, Beclin-1 autophagy related protein, apoptosis-related factor the Bcl-2, Bax and CytC protein were compared. Results: The rate of myocardial tissue apoptosis and the area of myocardial infarction in the pretreatment group and the model group were higher than those in the sham operation group, and the pretreatment group was lower than that in the model group (all P<0.05). The left ventricular end diastolic pressure (LVEDP) of rats in the pretreatment group and the model group was higher than that in the sham operation group, and the preconditioning group was lower than that in the model group (all P<0.05). The levels of maximum rate of pressure rise (+dp/dtmax) and the maximum rate of pressure decline (-dp/dtmax) in the left ventricle in the pretreatment group and model group were lower than those in the sham operation group, and the pretreatment group was higher than that in the model group (all P<0.05). Pretreatment group and model group rats P62, Beclin 1 protein expression levels were higher than those in sham operation group, and pretreatment group was lower than the model group (all P<0.05). The mRNA expression levels of Bcl-2 in the pretreatment group and the model group were lower than those in the sham operation group, and the pretreatment group was higher than that in the model group (all P<0.05). The mRNA expression levels of Bax and CytC protein expression levels in the pretreatment group and model group were higher than that in the sham operation group, and the pretreatment group was lower than that in the model group (all P<0.05). Conclusion: Rosuvastatin pretreatment can significantly reduce the degree of myocardial tissue damage in MIRI rats, and the main mechanism of action may be related to the effective inhibition of the expression of autophagy factors in myocardial cells and the regulation of apoptosis-related gene expression by rosuvastatin. |
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