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目的探讨颈动脉内膜切除术(CEA)后新内膜形成过程中细胞凋亡对早期再狭窄的影响。方法以新西兰兔颈动脉粥样硬化性狭窄动物模型为基础,分别采用免疫组织化学方法及原位末端标记(TUNEL)法观察颈动脉内膜切除术后不同时间点新内膜中Bax、Bcl-2动态表达及细胞凋亡的过程。结果Bax、Bcl-2在正常动脉壁无表达。Bcl-2于术后3 d内膜开始表达,术后30 d达到高峰,随后逐渐下降。Bax于术后3 d内膜开始表达。术后7 d到达高峰,随后逐渐下降,Bcl-2/Bax的比值在术后30 d达峰值。新内膜中细胞凋亡则在早期再狭窄的后期90 d达峰值。结论新内膜中细胞凋亡处于较活跃的水平,细胞凋亡在CEA术后早期再狭窄形成过程中有重要作用。
Objective To investigate the effect of apoptosis on the early restenosis during neointima formation after carotid endarterectomy (CEA). Methods Based on the animal model of carotid atherosclerosis in New Zealand rabbits, the expressions of Bax and Bcl-2 in the neointima of carotid endarterectomy were observed by immunohistochemical method and TUNEL method respectively. 2 dynamic expression and apoptosis process. Results Bax and Bcl-2 were not expressed in the normal artery wall. Bcl-2 began to express in the intima of the third day after operation, reached a peak on the 30th day after operation, and then decreased gradually. Bax began to be expressed within 3 days after operation. The peak was reached at 7 days after operation, and then gradually decreased. The ratio of Bcl-2 / Bax peaked at 30 days after operation. Apoptosis in neointima reached its peak at 90 days after the early restenosis. Conclusions Apoptosis in neointima is at an active level. Apoptosis plays an important role in the early restenosis after CEA.