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目的运用蛋白质组学技术探讨腹主动脉缩窄(AAC)高血压大鼠左室肥厚差异蛋白质表达及其在左室肥厚发生机制中的作用。方法 8周龄 SD 大鼠随机分为 AAC 组及假手术组,9周后行心脏超声、血流动力学、病理学检查,并对二组心肌组织行双向电泳(2DE)找出差异点,MALDI-TOF-MS 质谱鉴定蛋白质及 West-ern-blot 验证。结果 AAC 组心率、收缩压、舒张压、左室收缩末压、左室压力变化速率、室间隔厚度与左室后壁厚度及心质量、心质量/体质量较假手术组均显著增加(P<0.05),心肌细胞排列紊乱、细胞核增大、畸形、染色加深。2DE 中以浓度相差2倍以上为差异点,鉴定的21个蛋白质中,AAC 组相对于假手术组有14个蛋白质上调,4个蛋白质下调,3个蛋白为 AAC 组新出现,上调蛋白质包括:肌球蛋白轻链、心肌α肌动蛋白1蛋白原、β肌球蛋白重链、3磷酸甘油醛脱氢酶、线粒体核糖体蛋白 L15、G 蛋白偶联受体34、酪氨酸蛋白激酶 ZAP-70、RIKENcDNA 9030617003、天冬氨酸 tRNA 合成酶等,下调蛋白为 H~-转运 ATP 合成酶、L-3脂酰辅酶 A 脱氢酶等,两组蛋白表达差异有统计学意义(P<0.05)。结论 AAC 大鼠心肌中参与糖酵解蛋白、信号转导通路蛋白、基因表达调控蛋白增加,最终心肌细胞结构蛋白增加导致心肌肥厚。
Objective To investigate the differential expression of protein in left ventricular hypertrophy (AA) and its role in the pathogenesis of left ventricular hypertrophy in rats with abdominal aortic constriction (AAC) using proteomics. Methods Eight-week-old Sprague-Dawley rats were randomly divided into AAC group and sham operation group. Echocardiography, hemodynamics and pathology were performed 9 weeks later. Two groups of myocardial tissues were identified by two-dimensional electrophoresis (2DE) TOF-MS mass spectrometry identification of proteins and West-ern-blot validation. Results Heart rate, systolic blood pressure, diastolic blood pressure, left ventricular end-systolic pressure, left ventricular pressure change rate, interventricular septum thickness and left ventricular posterior wall thickness and heart mass, heart mass / body mass in AAC group were significantly higher than those in sham operation group <0.05), myocardial cells arranged in disorder, enlarged nucleus, deformity, staining deepened. 2DE in the concentration difference of more than 2 times the difference between the identified 21 proteins, AAC group compared with the sham group had 14 protein upregulation, 4 protein downregulation, 3 protein AAC group emerged, the up-regulation of proteins include: Myosin light chain, cardiac α-actin 1 -protein, β-myosin heavy chain, glyceraldehyde 3-phosphate dehydrogenase, mitochondrial ribosomal protein L15, G-protein coupled receptor 34, tyrosine protein kinase ZAP -70, RIKENcDNA 9030617003, aspartic acid tRNA synthetase, H-transport ATP synthase, L-3 acyl-CoA dehydrogenase and so on, the difference between the two groups was statistically significant (P < 0.05). Conclusion AAC rats are involved in the regulation of glycoprotein, signal transduction pathway proteins and gene expression regulatory proteins in the myocardium, resulting in myocardial hypertrophy resulting from the increase of myocardial structural proteins.