摘要
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。
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.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2008年第6期644-647,共4页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
湖南省自然科学基金项目(06JJ50051
06JJ30016)
湖南省教育厅科学研究项目(06C693)
