心肌肥大的机制:丝裂素活化蛋白激酶抑制剂对血管紧张素Ⅱ诱导心肌细胞血小板衍生生长因子受体表达的影响(英文)  

Mechanism of cardiac hypertrophy:Effect of mitogen activated protein kinase inhibitor on expression of platelet-derived growth factor receptor induced by angiotensin Ⅱin cardiac myocytes

作　　者：孙银平[1] 王省[2] 白桦[3] 邢东琦[3] 吴立玲[3] 

机构地区：[1]新乡医学院病理生理教研室,河南省新乡市453003 [2]新乡医学院解剖教研室,河南省新乡市453003 [3]北京大学医学部病理生理教研室,北京市100083

出　　处：《中国临床康复》2005年第7期186-187,共2页Chinese Journal of Clinical Rehabilitation

摘　　要：背景:血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)是诱导心肌肥大的强刺激因子,血小板衍生生长因子(platelet-derivedgrowthfactor,PDGF)也是致心肌肥大因素之一,AngⅡ是否可以通过诱导PDGF受体表达进一步促使心肌肥大?目的:探讨丝裂素活化蛋白激酶在AngⅡ致心肌细胞肥大的作用,为心肌肥大的防治提供理论依据。设计:以分离纯化培养的Wistar乳鼠心肌细胞为研究对象的对照性实验研究。单位:一所大学的病理生理教研室。材料:实验在北京大学医学院病理生理学实验室进行。实验动物为80只出生1～3d的Wistar乳鼠(北京大学医学部动物中心提供),雌雄不限。均在细胞培养室取出心脏做心肌细胞培养。干预:分离纯化培养的乳鼠心肌细胞,分为3组,以1×10-7mol/LAngⅡ刺激为AngⅡ组;以1×10-5mol/LPD98059(一种丝裂素活化蛋白激酶抑制剂)预孵育30min后再用AngⅡ刺激为PD98059组;以正常的乳鼠心肌细胞为对照组。培养24h后采用免疫印迹法测定每组心肌细胞PDGF-β受体的含量。主要观察指标:各组心肌细胞PDGF-β受体的含量。结果:AngⅡ刺激培养24h的乳鼠心肌细胞PDGF-β受体表达(432.41±54.08)和对照组(197.65±44.10)比较增强,差异有显著性意义(q=6.77,P<0.01),PD98059组PDGF-β受体表达(317.2±21.12)与AngⅡ组比较明显下降,差异?BACKGROUND:Angiotensin Ⅱ(AngⅡ) can induce cardiac hypertrophy and platelet-derived growth factor(PDGF) also stimulates cardiac hypertrophy.Is AngII responsible for the pathogenesis of cardiac hypertrophy by inducing PDGF receptor expression? OBJECTIVE:To investigate the effect of mitogen activated protein kinase(MAPK) on the role of cardiac hypertrophy induced by AngⅡin cardiac myocytes so as to provide theoretical basis for clinical prevention and cure of cardiac hypertrophy. DESIGN:Controlled experimental study taking cardiac myocytes of cultured neonatal rats as subjects. SETTING:Department of pathophysiology in a university. MATERIALS:The experiment was completed in the Department of Pathophysiology,Medical College of Peking University.A total of 80 Wistar rats of either gender,aged 1-3 days,were provided by the Animal Center of Medical College,Peking University.Their hearts were removed for myocyte culture in the Cell Culture Laboratory. INTERVENTIONS:The cultured neonatal rat cardiac myocytes treated with 10-7mol/L AngⅡwere AngⅡgroup,and those preincubated with 10-5mol/L PD98059(an antagonist of MAPK)for 30 minutes and then treated with AngⅡwere PD98059 group.Cardiac myocytes of normal neonatal rats were as control group.The expression of PDGF-βwas detected by western blot at 24 hours. MAIN OUTCOME MEASURES:Content of PDGF-βreceptor in neonatal rat cardiac myocytes. RESULTS:The expression of PDGF-βreceptor induced by AngⅡat neonatal rat cardiac myocytes markedly increased at 24 hours (432.41 ±54.08) compared with that of control group(197.65±44.10)(q=6.77,P< 0.01).PDGF-βreceptor expression of PD98059 group(317.2±21.12)decreased compared with that of AngⅡgroup(q = 3.91, P< 0.05). However,the expression did not return to the level of control group, and there was significant difference between PD98059 group and control group(q = 3.85,P< 0.05). CONCLUSION:The results indicate that angiotensin II promotes cardiac hypertrophy through inducing expression of PDGF receptor, in which

关 键 词：心肌/代谢 受体 血小板源生长因子 蛋白激酶类 血管紧张素Ⅱ 细胞 培养的 

分 类 号：R542.2[医药卫生—心血管疾病]