中文摘要：

观察外源性SM22α对球囊损伤诱导的大鼠颈总动脉新生内膜形成的影响，并探讨其机制。雄性SD大鼠经球囊剥脱颈总动脉内皮后随机分为3组：未感染组、pAd组和pAd—SM22α组。术后14天取颈总动脉标本，HE染色观察血管内膜增生情况，用Western blot和免疫组化方法检测外源性SM22α、PCNA和p27在血管壁中的表达水平，以及Raf-1、MEK1／2和ERK1／2的磷酸化水平。实验结果显示，外源性SM22α在血管壁中得到稳定表达；过表达SM22α可显著抑制球囊损伤诱导的血管新生内膜的增厚，与pAd组比较，内膜／中膜比值（I／M）降低70％；Western blot结果显示，在pAd—SM22α组中增殖标志物PCNA表达水平降低（P〈0．05），而增殖抑制蛋白p27表达水平增高（P〈0．05），同时伴有增殖相关信号转导分子Raf-1、MEK1／2和ERK1／2的磷酸化水平降低（P〈0．05）。结果提示，过表达SM22α可抑制球囊损伤诱导的血管内膜增生，其机制可能与阻断Raf-1．MEK1／2．ERK1／2通路的级联活化有关。

英文摘要：

To observe the effect of SM22α on neointimal hyperplasia after balloon injury and to investigate its mechanism of action, male SD rats were randomly divided into three groups after balloon injury, including uninfected group, pAd group and pAd-SM22α group. All rats were killed after 14d and carotid arteries were removed. Neointima thickening was assessed using HE staining. Western blot and immunohistochemistry were used to detect SM22α, PCNA and p27 expression in the vascular wall. The phosphorylation of Raf-1, MEK1/2 and ERK1/2 was examined by Western blot. The results showed that pAd-SM22α stably expressed SM22α protein in the transfected vascular wall. Overexpression of SM22α significantly inhibited neointimal hyperplasia induced by balloon injury. The expression of PCNA protein in pAd-SM22α group was decreased compared with the control （P〈0.05）. Meanwhile, the expression of p27 protein in pAd-SM22α group was significantly increased （P〈0.05）.The phosphorylation of Raf-1, MEK1/2 and ERK1/2 in the pAd-SM22α group was decreased （P〈0.05）, with reduction of neointimal hyperplasia. This study suggests that SM22α inhibits neointimal formation after balloon injury in rats via the blockade of Raf-I-MEK1/2-ERK1/2 signaling pathway.