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AIM:To study the effect of cromakalim(Cro)on proliferation and apoptosis of vascular smooth muscle cells(VSMCs)in spontaneously hypertensive rats(SHR).METHODS:Thirty SHR(12 weeks old) were randomly divided into two groups(Cro group and SHR group)and ten WKY(12 weeks old)were control group.Cro group was given Cro(0.6 mg·kg~(-1)·d~(-1),twice per day)for 16 weeks and the other two groups were given placebo for 16 weeks.The expression of Bcl-2,Bax and PCNA protein were determined by immunohisto- chemical staining.VSMCs...

AIM:To study the effect of cromakalim(Cro)on proliferation and apoptosis of vascular smooth muscle cells(VSMCs)in spontaneously hypertensive rats(SHR).METHODS:Thirty SHR(12 weeks old) were randomly divided into two groups(Cro group and SHR group)and ten WKY(12 weeks old)were control group.Cro group was given Cro(0.6 mg·kg~(-1)·d~(-1),twice per day)for 16 weeks and the other two groups were given placebo for 16 weeks.The expression of Bcl-2,Bax and PCNA protein were determined by immunohisto- chemical staining.VSMCs apoptosis was identified by in situ TdT-mediated dUTP nick end labeling(TUNEL) and smooth muscle cell apoptotic index(SMAI)was calculated by semi-quantitative analysis.RESULTS: Compared with control group,systolic blood pressure of SHR group increased significantly(P<0.05),the ex- pression of Bcl-2 and PCNA protein increased(P<0.05),SMAI decreased(P<0.01),but there were no sig- nificant difference in Bax expression.Compared with SHR group,systolic blood pressure of Cro group was trend to decrease(P>0.05),expression of Bcl-2 and PCNA protein decreased(P<0.05),the ratio of Bcl-2/Bax were significantly lower,SMAI was increased significantly(P<0.05).CONCLUSION:The mechanism that cromakalim promote the apoptosis of VSMCs in SHR may be involved the expression balance of Bcl-2/Bax in VSMCs.

目的:观察色满卡林对自发性高血压大鼠(SHR)血管平滑肌细胞(VSMCs)凋亡的影响。方法:30只12 wk龄SHR,随机分为高血压组、色满卡林组,另设正常对照组。色满卡林组给予色满卡林0.6 mg·kg~(-1)·d~(-1),分2次灌胃;另2组每日给予等量的生理盐水,共16 wk。监测尾动脉收缩压。用免疫组化法检测Bcl-2,Bax和PCNA蛋白表达。荧光标记TUNEL法检测VSMCs凋亡,计算VSMCs凋亡指数(SMAI)。结果:高血压组与正常对照组比较,收缩压明显增高(P<0.05);VSMCs中的Bcl-2,PCNA蛋白表达明显增强(P<0.05);SMAI明显减少(P<0.01);Bax蛋白表达2组间差异无显著意义(P>0.05)。与高血压组比较,色满卡林组尾动脉收缩压呈降低趋势,但差别无显著意义(P>0.05);VSMCs的Bcl-2和PCNA蛋白的表达减少(P<0.05),Bcl-2/Bax比值下降;SMAI增加(P<0.05)。结论:色满卡林促进了SHR的VSMCs凋亡,可能机制是通过调节VSMCs的Bcl-2/Bax蛋白表达平衡。

 
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