| 引用本文: |
李琪琳,胡元会,霍艳明,王辉奇,王强,王欢.卡托普利干预心力衰竭大鼠心肌线粒体蛋白质组学研究[J].湖南中医药大学学报,2018,38(10):1104-1109[点击复制] |
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| 卡托普利干预心力衰竭大鼠心肌线粒体蛋白质组学研究 |
| 李琪琳,胡元会,霍艳明,王辉奇,王强,王欢 |
| (中国中医科学院望京医院, 北京 100102;中国中医科学院广安门医院, 北京 100053) |
| 摘要: |
| 目的 研究卡托普利对心衰大鼠心肌线粒体蛋白质组学的影响。方法 SD大鼠随机分为造模组与假手术组；造模组采用结扎冠脉致心梗后心衰模型，术后再随机分为模型组、卡托普利组；各组连续予以相应干预8周后采集大鼠心肌，采用双向凝胶电泳和质谱技术，分析各组大鼠心肌线粒体蛋白质组学变化，并运用Western blot技术对差异蛋白进行回复性验证。结果 模型组与假手术组相比有差异，且卡托普利能使差异趋势逆转的蛋白点为19个，其中11个表达上调，8个表达下调；经质谱分析成功鉴定出12个蛋白，主要涉及能量代谢、氧化损伤、应激反应、细胞骨架、细胞分化增殖等功能。Western blot结果显示模型组ATP-α表达下调，Stress-70、Nucleophosmin表达上调；卡托普利组ATP-α表达上调，Stress-70、Nucleophosmin表达下调，与蛋白质组学结果基本一致。结论 卡托普利可一定程度调节心衰大鼠心肌线粒体蛋白质组学变化，其干预机制可能与改善能量代谢、抗氧化损伤、减轻应激反应及调节细胞分化增殖等功能相关。 |
| 关键词: 卡托普利 心力衰竭 心肌线粒体 蛋白质组学 |
| DOI：10.3969/j.issn.1674-070X.2018.10.003 |
| 投稿时间：2018-09-11 |
| 基金项目:北京市自然科学基金项目（7122154）。 |
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| Effect of Captopril on Myocardial Mitochondrial Proteomics in Rats with Heart Failure |
| LI Qilin,HU Yuanhui,HUO Yanming,WANG Huiqi,WANG Qiang,WANG Huan |
| (Wangjing Hospital of China Academy of Chinese Medical Sciences, Beijing 100102, China;Guang'anmen Hospital of China Academy of Chinese Medical Sciences, Beijing 100053, China) |
| Abstract: |
| Objective To investigate the effect of captopril on myocardial mitochondrial proteomics in rats with heart failure and its possible mechanism. Methods Sprague-Dawley rats were randomly divided into sham-operation group and modeling group. The rats in the modeling group were treated with ligation of the coronary artery to induce myocardial infarction and to establish a model of heart failure. Then, the model rats were randomly divided into model group and captopril group. After 8 weeks of drug intervention, the changes in mitochondrial proteomics of myocardial tissue were analyzed by two-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). Furthermore, the expression levels of differentially expressed proteins were verified by Western blot. Results There were significant differences in the levels of some proteins between the model group and the sham-operation group (P<0.05). The changes in the levels of 19 differentially expressed proteins (11 with up-regulated expression and 8 with down-regulated expression) between the model group and the sham-operation group were reversed in the captopril group; 12 differentially expressed proteins were successfully identified by MALDI-TOF-MS. Bioinformatics analysis showed that these differential proteins were mainly associated with energy metabolism, oxidative damage, stress response, cytoskeleton, and cell differentiation and proliferation. Western blot results showed that compared with the sham-operation group, the model group had significantly reduced expression of ATP-α and significantly increased expression of stress-70 protein and nucleophosmin; compared with the model group, the captopril group had significantly increased expression of ATP-α and significantly reduced expression of stress-70 protein and nucleophosmin. The results were consistent with those in proteomics. Conclusion Captopril can partly adjust the changes in myocardial mitochondrial proteomics in rats with heart failure, and its intervention mechanism may involve improving energy metabolism, anti-oxidative damage, and alleviating stress response, as well as regulating cell differentiation and proliferation. |
| Key words: captopril heart failure myocardial mitochondria proteomics |
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