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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
【摘要】 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。
【Abstract】 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 immunohistochemical 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 interlobular 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<0.01). 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.
【Key words】 Hypertension/pathology Mitogen-Activated protein kinases Genes; jun Immunohistochemistry Gene expression Animals laboratory Rats; wistar;
- 【文献出处】 陕西医学杂志 ,Shaanxi Medical Journal , 编辑部邮箱 ,2005年08期
- 【分类号】R544.1
- 【被引频次】8
- 【下载频次】170