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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。
To observe the effect of exogenous SM22α on the neointimal hyperplasia of carotid artery induced by balloon injury in rats and its mechanism. The male SD rats were randomly divided into three groups: uninfected group, pAd group and pAd-SM22α group. The specimens of common carotid arteries were taken 14 days after operation and the intimal hyperplasia was observed by HE staining. The expressions of exogenous SM22α, PCNA and p27 in the vascular wall were detected by Western blot and immunohistochemistry, and the expressions of Raf-1, MEK1 / 2 and ERK1 / 2 phosphorylation levels. The experimental results showed that exogenous SM22α was stably expressed in the vascular wall. Overexpression of SM22α significantly inhibited balloon injury-induced neointimal hyperplasia. Compared with the pAd group, the ratio of intima / media (I / M ) Decreased by 70%. Western blot showed that the expression of PCNA was decreased in pAd-SM22α group (P <0.05), while the expression of p27 was increased (P <0.05), accompanied by proliferation-related signal transduction The phosphorylation levels of Raf-1, MEK1 / 2 and ERK1 / 2 were decreased (P <0.05). The results suggest that over-expression of SM22α can inhibit balloon injury-induced intimal hyperplasia, which may be related to the blockade of cascade activation of Raf-1-MEK1 / 2-ERK1 / 2 pathway.