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一氧化氮抑制内皮素促血管平滑肌细胞增殖作用的信号转导途径

郑惠珍, 安国顺, 聂思槐, 唐朝枢, 刘乃奎, 王述恒

北京医科大学心血管基础研究所；广东医学院生理学教研室

摘要

培养的家兔胸主动脉血管平滑肌细胞（VSMC）分别以内皮素（ET-1）、一氧化氮（NO）前体L-Arg和NO供体SIN-1刺激，或用ET-1＋L-Arg、ET-1＋SIN-1联合刺激，测VSMC3H-TdR掺入、丝裂素活化蛋白激酶（MAPK）活性及蛋白激酶C（PKC）活性的改变，以研究NO抑制ET-1促VSMC增殖作用的信号转导途径。结果表明：（1）ET-110－8mol／L单独刺激，3H-TdR掺入、MAPK活性、PKC活性分别较对照组增加5倍、4倍和3倍（P＜0．01）；L-Arg或SIN-1刺激对上述指标无明显影响；（2）ET-1与L-Arg（2、5、10nmol／L）联合刺激，3H-TdR掺入、MAPK活性和PKC活性均明显低于ET-1单独刺激组；（3）ET-1与SIN-1（5、10、50μmol／L）联合刺激，3H－TdR掺入、MAPK活性和PKC活性也均明显低于ET-1单独刺激组。结果提示：NO抑制ET-1促VSMC增殖的作用，此作用与NO抑制ET-1激活PKC、MAPK活性终止ET-1的细胞内信号转导途径有关。

关键词： 一氧化氮; 内皮素; 丝裂素活化蛋白激酶; 蛋白激酶C; 血管平滑肌细胞; 细胞增殖

Cui Hong

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

Abstract

The signal transduction pathways of the inhibitory effect of nitric oxide (NO) on endothelin (ET)-induced proliferation of vascular smooth muscle cells (VSMCs) were studied.3H-thymidine(TdR) incorporation, mitogen-activated protein kinase (MAPK)activity and protein kinase C (PKC) activity of cultured VSMCs of rabbits thoracic aorta were measured in the presence of either NO precursor L-arginine (L-Arg) or NO donor 3 morpholino sydnonimine-hydrochloride (SIN-1), or ET-1 alone or with L-Arg or SIN-1.The results show: (1) ET-1 (10-8 mol/L) significantly increased VSMCs 3H-TdR incorporation (5 times, P <0.01), MAPK activity (4 times, P < 0.01) and PKC activity (3 times, P <0.01 ), as compared with control. L-Arg or SIN-1 alone was without effect on 3H-TdR incorporation, MAPK activity and PKC activity. (2) When ET1 and L-Arg (2, 5, 10 mmol/L) were simultaneously administered, 3H-TdR incorporation and activity of both MAPK and PKC were all significantly dacreased in comparison with the ET group.

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引用本文：

郑惠珍, 安国顺, 聂思槐, 唐朝枢, 刘乃奎, 王述恒. 一氧化氮抑制内皮素促血管平滑肌细胞增殖作用的信号转导途径[J]. 生理学报 1998; 50 (4): .

Cui Hong. . Acta Physiol Sin 1998; 50 (4): (in Chinese with English abstract).