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大鼠压力负荷性肥大心肌中TNF-αmRNA表达变化

Expression of TNF-α mRNA in hypertrophic myocardium by pressure overload in rats

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【作者】 苏兴利高广道罗秀成王佐贤王新凤刘进军林元喜

【Author】 SU Xing-li~2, GAO Guang-dao~1, LUO Xiu-cheng~2, WANG Zuo-xian~2, WANG Xin-feng~1, LIU Jin-jun~1, LIN Yuan-xi~1(~1Department of Pathophysiology, Medical College of Xi’an Jiaotong University, Xi’an 710061, China;?~2?Department of Pathophysiology, Shanxi Medical College, Xi’an 710068, China)

【机构】 陕西医学高等专科学校病理生理教研室西安交通大学医学院病理生理教研室西安交通大学医学院病理生理教研室 陕西西安710068陕西西安710061陕西西安710068陕西西安710061

【摘要】 目的 :探讨大鼠压力负荷性肥大心肌中TNF -αmRNA表达的变化及卡托普利 (captopril)对其的影响。方法 :采用腹主动脉缩窄法复制压力超负荷心肌肥大模型 ,于术后 4 2d采血、摘取心脏 ,测定心肌肥大指数并采用酶联免疫法测定血清及左心室肌TNF -α含量 ;应用心肌原位杂交法结合图像分析系统检测心肌组织中TNF -αmRNA表达的变化 ,并观测TNF -αmRNA在心肌组织中的定位。结果 :术后 4 2d心肌明显肥大 ,以左心室为主 ;主动脉缩窄 (aorta -constriction ,AC)组心室肌TNF -α含量比假手术 (sham -operation ,SO)组高 98% (P <0 0 1) ;卡托普利干预使心室肌TNF -α含量比AC组低 6 4 14 % (P <0 0 1) ,但未达到对照水平 ;心肌组织原位杂交显示TNF -αmRNA表达主要在心肌间质部位 ,假手术组心肌TNF -αmRNA表达水平极低 ,明显低于AC术后 (P <0 0 1) ,captopril干预虽明显抑制AC术后心肌组织中TNF -αmRNA表达 ,但并未使其达到SO组水平。结论 :心肌组织内源性TNF -α的表达增加在压力负荷性心肌肥大中具有重要的调控作用 ,其过表达可能与RAS激活促心肌间质TNF -αmRNA表达上调有关

【Abstract】 AIM: To observe the change of TNF-α mRNA in hypertrophic cardiac myocytes induced by pressure overload in rats and the effect of captopril. METHODS: Serum and heart were collected 42 days after the cardiac hypertrophy model made by pressure overload by abdomen aorta-constriction (AC). Hypertrophic parameter and the concentration of TNF-α in serum and left ventricle were determined by ELISA. TNF-α mRNA in cardiac myocytes was determined by in situ hybridization and analyze by ELIA image analysis system. The orientation of (TNF-α) mRNA in cardiac myocytes was also observed. RESULTS: Left ventricle hypertrophy was observed 42 days after operation. TNF-α mRNA in AC group elevated 98% compared to sham-operated group and descended 64.14% by captopril ((P<0.01),) but did not descend to the normal level. The expression of TNF-α mRNA showed mostly in myocardial matrix by in situ hybridization. The level of expression was very low in sham-operation group and markedly enhanced after aorta-constriction, but it was decreased when treated by captopril. CONCLUSION: Endogenous TNF-α acts as an important adjustive factor in the pressure overload-induced cardiac hypertrophy and TNF-α mRNA increased in myocardial matrix may be activated by renin-angiotension system.

【关键词】 心肌肥大肿瘤坏死因子卡托普利大鼠
【Key words】 MyocardiumHypertrophyTumor necrosis factorCaptoprilRats
【基金】 陕西省卫生厅资助项目 (No.2 0 0 0 0 9)
  • 【文献出处】 中国病理生理杂志 ,Chinese Journal of Pathophysiology , 编辑部邮箱 ,2004年08期
  • 【分类号】R363
  • 【被引频次】4
  • 【下载频次】104
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