ISSN 0371-0874, CN 31-1352/Q

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缺血-再灌注时大鼠心脏Gi蛋白α亚基的变化

王瑶, 吴立玲, 葛明珠

北京医科大学病理生理教研室. 北京 100083

摘要

本工作研究了心肌缺血-再灌注时,受体-腺苷酸环化酶细胞膜信号转导系统中G蛋白含量及功能的变化。采用免疫印迹法和放射免疫法分别测定大鼠心脏Gia2,Gia3和Gsa的含量及腺苷酸环化酶的活性。结果显示缺血-再灌注时心功能明显损伤;心脏Gsa无明显变化;心肌细胞膜Gia2和Gia3含量分别升高37.4%(P<0.01)和42.4%.(P<0.01);胞浆内Gia2和Gia3含量无明显变化;缺血心肌腺苷酸环化酶活性降低。上述结果提示,缺血-再灌注时可引起心脏抑制性G蛋白升高,导致腺苷酸环化酶信号转导系统功能障碍及心功能异常的发生。

关键词: G蛋白; 缺血-再灌注; 信号转导; 腺苷酸环化酶

Cui Hong

First Clinical Institute,China Medical University. Shenyang 110001,Liaoning, China

Abstract

Alteration of G proteins in rat heart during ischemia-reperfusion was studied. Levelsof Cia2, Gia3 and Gsa in sarcolemma and light vesicle were measurdd by Westem blotanalysis. Adenyl cyclase activities were determined by radioimmunoassay. Duringischemia-reperfusion, cardiac function parameters were decreased significantly.Expressions of Gsa remained unchanged. Compared with the control group, levels of Gia2and Gia3 in sarcolemma in ischemia-reperfusion group increased by 37 .4% (P<0.01)and 42.4% (P<0.01), respectively with, however, no changes in light vesicle;Activities of adenyl cyclase decreased during ischemia-reperusion. The results suggestedthat the increased expression of cardiac Gi may contribute to the dysfunction of adenylcyclase signal transduction system and the impaired cardiac function during ischemiareperfusion.

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引用本文:

王瑶, 吴立玲, 葛明珠. 缺血-再灌注时大鼠心脏Gi蛋白α亚基的变化[J]. 生理学报 1998; 50 (5): .

Cui Hong. . Acta Physiol Sin 1998; 50 (5): (in Chinese with English abstract).