维拉帕米诱导血管平滑肌细胞凋亡及其在再狭窄机制中的作用

Vascular smooth muscle cell apoptosis induced by verapamiland the effect of cell apoptosis in the mechanism ofrestenosis after angioplasty

目的探讨维拉帕米能否诱导血管平滑肌细胞凋亡及细胞凋亡在再狭窄机制中的作用。方法分别取正常兔髂动脉，动脉粥样硬化及再狭窄髂动脉血管中膜组织进行平滑肌细胞培养，［３Ｈ］ＴｄＲ参入法测定细胞增殖活性，维拉帕米诱导平滑肌细胞凋亡，通过电镜观察，ＤＮＡ凝胶电泳及流式细胞仪了解各组平滑肌细胞凋亡情况。结果维拉帕米诱导下，平滑肌细胞的变化具有凋亡的典型特征。血管成形术后，细胞增殖及凋亡系统均被激活，再狭窄组细胞增殖程度增加２６％，细胞凋亡激活程度增加１９％，二者比例失衡。结论维拉帕米能够引起血管平滑肌细胞凋亡，而平滑肌细胞凋亡的相对减少在再狭窄的发生机制中发挥一定的作用。

AIM To investigate whether verapamil could induce vascular smooth muscle cell apoptosis and the effect of cell apoptosis in the mechanism of restenosis after angioplasty. METHODS Rabbit iliac artery atherosclerotic and restenotic models were made. The normal, atherosclerotic and restenotic iliac arteries were aseptically removed from rabbits for the cultures of iliac artery smooth muscle cell(SMC) respectively. Cell proliferation was examined with TdR incorporation and cell apoptosis was investigated in SMC treated with verapamil through the observation of cell morphology, DNA gel electrophoresis and flow cytometry. RESULTS The findings showed that the extent of proliferation activated increased by 26% and the extend of apoptosis activited increased by 19%; this might tip the balance between the two processes and the deletion of excessive SMC could not be made timely, thus, the restenosis will occur. CONCLUSIONTBZVerapamil can induce vascular smooth muscle apoptosis and SMC apoptosis may be involved in the pathogenesis of atherosclerotic and restenotic lessions; cell apoptosis activated to a lesser extent may play an improtant role in the mechanism of restenosis.