高血压大鼠血管平滑肌细胞中细胞外信号调节激酶和c-jun及凋亡相关基因的表达

The expression of extracellular signal-regulated kinase,c-jun and apoptosis relative genes in vascular smooth muscle cell in hypertensive rats

目的:探讨血管平滑肌细胞(VSMC)在高血压中的作用及其机制。方法:Wis-tar大鼠两肾一夹型高血压模型,采用免疫组织化学方法,观察肾细小动脉平滑肌细胞中ERK-2、c-jun和bax及bcl-6表达。结果:实验期间,高血压大鼠血压从112±18mmHg升高到实验结束时的198±33mmHg;高血压组肾小叶间动脉ERK-2染色阳性率(16.86%)明显高于对照组(P<0.01),入球动脉、小叶间动脉、叶间动脉和弓形动脉VSMC中ERK-2染色阳性率均明显高于对照组(P<0.01);高血压组入球动脉、小叶间动脉和弓形动脉VSMC中c-jun的阳性率明显高于对照组(P<0.01);高血压组肾弓形动脉及叶间动脉VSMC中bax染色阳性率均明显低于对照组(P<0.01);高血压组肾小叶间动脉bcl-6染色阳性率(12.96%)明显高于对照组(P<0.01),入球动脉、小叶间动脉VSMC中bcl-6阳性率均明显高于对照组(P<0.05)。结论:两肾一夹型高血压时,少数肾小动脉血管平滑肌细胞ERK-2过表达,使得转录相关基因c-jun等活化,凋亡基因抑制,最终使VSMC增多导致血管重构。

Objective ： To explore the effect and its molecular mechanism of vascular smooth muscle cell （VSMC） in hypertension . Methods：The expression of extracellular signal-regulated kinsae-2 （ERK-2）, c-jun, bax and bcl-6, was observed by means of immunohiatochemical technique in VSMC of renal small arteries and arterioles in two kidney-one clip hypertension Wistar rats. Results： During the experiment, blood pressure was raised significantly in the hypertension rats from the beginning 112±18mmHg to 198±33mmHg in the end . ERK-2 positive immunostaining rate of interlobula. arteries in the hypertension （16. 86%） was significantly higher than that of the control（P〈0, 01）; The rate of positive ERK-2 staining in VSMC of afferent arterioles, interlobular , interlobar and arch arteries was significantly higher than that of the control （P〈0. 01）, The rate of c-jun positive staining in the VSMC of afferent arterioles, interlobular and arch arteries was significantly higher than that of the controls （P〈0. 01 ）.In the hypertension rats, the positive staining rate of bax in the VSMC of arch and interlobar arteries was significantly lower than that of the control （P〈0.01）. The positive staining rate of bcl-6 in hypertension interlobular is higher than that of the control （P〈O. 01）. The positive staining of bcl-6 in VSMC of afferent and interlobular arteries of the hypertension was significantly higher than that of the control （P〈0. 05）. Conclusion： In two kidney-one clip hypertensive rats, overexpressing of ERK-2 activates some transcription relative genes, such as c-jun, decreases the apoptosis, and induces the VSMC to increase, which might play an important role in vascular remodeling in hypertension.