雷帕霉素抑制增生内膜中基质细胞衍生因子-1的表达

目的：进一步探讨雷帕霉素抗血管内再狭窄的分子机制。方法：球囊拉伤大鼠颈总动脉建立血管内膜增生的动物模型,口服雷帕霉素（25mg/kg）,4周后处死动物。HE染色观测血管病变,免疫组化检测增生内膜中基质细胞衍生因子-1（SDF-1）的表达,小室迁移系统观察SDF-1对平滑肌细胞迁移的影响。结果：球囊拉伤明显诱导血管内膜增生,增生内膜中有明显的SDF-1的表达,雷帕霉素能显著下调增生内膜中SDF-1的表达,而SDF-1浓度依赖性地诱导平滑肌细胞的迁移。结论：雷帕霉素可能通过下调SDF-1的表达从而抑制血管再狭窄。

Inhibitory effect of rapamycin on stromal cell-derived factor-1 expression in intimal hyperplasia

AIM： To investigate the anti-restenosis molecular mechanism of rapamycin.METHODS： The animal models of rat carotid artery intimal hyperplasia was established with Balloon injury.Rats were randomized divided into two groups： baseline group（n=10） and treatment group（n=10 rapamycin,25 mg/kg）.HE staining was used to observe vascular lesions.Immunochistochemistry staining was used to detect the expression of SDF-1 in lesions.The migration of smooth muscle cells induced by stromal cell-derived factor 1（SDF-1） was observed with transwell.RESULTS： Intimal hyperplasia was obviously induced by balloon injury.SDF-1 highly expressed in lesions and rapamycin significantly reduced the expression of SDF-1 in intimal hyperplasia.SDF-1 induced the migration of smooth muscle cells with concentration-dependent manner.CONCLUSION： Rapamycin may inhibit vascular restenosis by inhibiting the migration of smooth muscle cells induced by SDF-1.