摘要
目的 探讨大鼠胸主动脉内膜剥脱后内膜增生中苯那普利对血管平滑肌细胞凋亡及相关基因Fas抗原和Fas配体的影响。方法 5 2只大鼠随机分为假手术组 8只 ,苯那普利组和对照组各2 2只。后两组大鼠行胸主动脉内膜剥脱术 ,苯那普利组动物于术前 7天至术后 14天每日接受苯那普利 (10mg·d-1·kg-1)治疗。术后 14天处死 ,用免疫组化法测定Fas抗原与Fas配体在血管中的表达 ,原位末端标记法测定凋亡细胞。结果 内膜损伤后第 14天在新生内膜中有平滑肌细胞凋亡 ;苯那普利显著增加新生内膜中Fas抗原与Fas配体的表达 ,增加血管平滑肌细胞凋亡 ,减少新生内膜面积。结论 苯那普利可能通过Fas系统调节动脉血管内皮损伤修复过程中血管平滑肌细胞凋亡 ,而抑制新生内膜形成。
Objective To investigate the influence of benazepril on the apoptosis and related gene Fas antigen and Fas ligand (FasL) of vascular balloon injury in animal models. Methods Fifty two rats were divided randomly into artificial group ( n =8), control group ( n =22) and benazepril group ( n =22, 10 mg·kg -1 ·d -1 ). We made balloon endothelium denudation in thoracic aortae of rats in the latter two groups. The benazepril treatments had begun 7 days before balloon injury and continuously until the animals were killed 14 days after balloon injury. Fas and FasL were detected by immunohistochemistry in all rats. Apoptotic cells were stained in situ by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL). Results Apoptotic cells were present in the neointima of day 14 after vascular balloon injury and increased significantly by benazepril ( P< 0 001). Benazepril increased the expression of Fas and FasL in the neointima and attenuated the neointima area. Conclusion Benazepril may probably regulate the apoptosis after vascular balloon injury through Fas system and then inhibit the neointima hyperplasia.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
2000年第2期132-134,共3页
Chinese Journal of Cardiology
基金
河南省重大科技攻关项目!(971200100)
