中文摘要：

目的：探讨逆转录病毒介导的E1A激活基因阻遇子（CREG）过表达对球囊损伤后大鼠颈动脉新生内膜形成的影响。方法：以球囊拉伤法制备大鼠颈动脉损伤模型，应用Pluronic F127胶分别包裹含有pLNCX／CREG、pLNCX／GFP载体的逆转录病毒，并于损伤即刻涂抹于血管外壁。随后在损伤不同时点取出损伤动脉，测量内膜面积及内膜／中膜面积比。用免疫组织化学法观察CREG、SMα-actin及Ki-67变化，Westernblotting检测CREG蛋白表达。结果：血管损伤后2dpLNCX／GFP组血管中膜平滑肌层GFP表达。pLNCX／CREG组大鼠血管CREG表达明显多于单纯损伤组。感染CREG组大鼠球囊损伤后血管新生内膜的形成明显受抑，Ki-67蛋白表达明显少于、而SMα-actin表达则明显多于单纯损伤组。结论：CREG过表达能抑制血管损伤后平滑肌细胞的增殖并促进其分化，提示调控CREG基因的表达可能为预防PCI术后再狭窄提供有效手段。

英文摘要：

AIM ： To evaluate the effects of over - expression of cellular repressor of E1A - stimulated genes （CREG） mediated by retrovirus on neointima formation in injured rat carotid. METHODS： The pluronic F127 containing pLNCX/CREG or pLNCX/GFP retroviral vectors was placed around the injured rat carotid. The neointima, media areas and the intima to media ratio were calculated. Expressions of CREG, SM α - actin and Ki - 67 were detected. RESULTS ： The GFP expression was observed at day 2 in pLNCX/GFP groups. The expression of exogenous CREG was also significantly increased in arteries at day 2 after pLNCX - CREG infection. Over - expression of CREG significantly suppressed neointima formation, attenuated the expression of Ki - 67 and up - regulated SM α - actin expression. CONCLUSION ： Overexpression of CREG inhibits VSMCs proliferation and promotes VSMCs differentiation after vascular injury. It suggests that modulation of CREG expression or activity may be a viable approach to treat neointimal restenosis after percutaneous coronary intervention.