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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

孙银平 王省 白桦 邢东琦 吴立玲

中国临床康复2005,Vol.9Issue(7):186-187,2.
中国临床康复2005,Vol.9Issue(7):186-187,2.

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

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

孙银平 1王省 2白桦 3邢东琦 3吴立玲3

作者信息

  • 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
  • 折叠

摘要

Abstract

BACKGROUND: Angiotensin Ⅱ (Ang Ⅱ) 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 Ang Ⅱ in 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 Ang Ⅱ were Ang Ⅱ group, and those preincubated with 10-5mol/L PD98059(an antagonist of MAPK) for 30 minutes and then treated with Ang Ⅱ were PD98059 group. Cardiac myocytes of normal neonatal rats were as control group. The expression of PDGF-β was detected by western blot at 24 hours.MAIN OUTCOME MEASURES: Content of PDGF-β receptor in neonatal rat cardiac myocytes.RESULTS: The expression of PDGF-β receptor induced by Ang Ⅱ at 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-β receptor expression of PD98059 group(317.2 ± 21.12) decreased compared with that of Ang Ⅱ group(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 mitogen activated protein kinase participates in. Maybe it is another important mechanism for Ang Ⅱ -induced cardiac hypertrophy. The results can provide experimental data for the primary and secondary prevention in heart rehabilitation.

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

医药卫生

引用本文复制引用

孙银平,王省,白桦,邢东琦,吴立玲..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[J].中国临床康复,2005,9(7):186-187,2.

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