旋覆花素抑制血管内皮剥脱诱导的粘附分子表达

目的观察旋覆花素对内皮剥脱诱导的新生内膜形成过程中血管壁粘附分子OPN、ICAM-1、ILK表达的影响,为寻找该药物抑制新生内膜形成的作用靶标提供实验依据。方法采用主动脉球囊损伤后血管狭窄动物模型,用免疫组织化学和Western Blot方法分别检测血管壁中骨桥蛋白(osteopontin,OPN)、细胞间粘附分子-1(intercellular adhesion molecule-1,ICAM-1)、整合素偶联激酶(integrin-linked kinase,ILK)的表达变化及旋覆花素对其的影响。结果血管内皮剥脱可诱导血管壁平滑肌细胞大量增生,新生内膜呈弥漫性增厚,血管损伤局部组织中OPN、ICAM-1、ILK的表达均比正常对照组明显升高(P<0.05)。旋覆花素治疗组在球囊损伤后,血管内膜增生程度显著减轻,血管壁OPN、ICAM-1、ILK的表达均比模型组明显降低(P<0.05)。结论旋覆花素减缓新生内膜形成的效应与其抑制粘附分子的表达、阻断粘附分子信号传递有关。

ACETYLBRITANNILACTONE INHIBITS ADHESION MOLECULE EXPRESSION IN NEOINTIMA FORMATION AFTER BALLOON INJURY

Objective To study the relationship between the neointima formation and the adhesion molecule expression in rat aorte after balloon injury,and the effect of acetylbritannilactone on neointima formation.Methods The model of vascular restenosis was established by balloon injury.Immunohistochemistry and Westernblot were used to detect the changes of OPN,ICAM-1 and ILK expressions in vascular tissues after balloon injury.Results The neointima thickness in the model group was significantly higher than that in the control group at 21 days after balloon injury(P<0.05).As compared with that of the control group,the expression activity of OPN,ICAM-1 and ILK in the vascular wall was enhanced significantly in the model group.Acetylbritannilactone treatment resulted in mild intimal hyperplasia and decrease in expression level of OPN,ICAM-1 and ILK.(P<0.05).Conclusion Acetylbritannilactone can significantly inhibite neointima formation by suppressing the expression of OPN,ICAM-1 and ILK.