摘要
目的研究在人脐静脉内皮细胞中3-羟-3-甲基戊二酰辅酶 A(HMG-CoA)还原酶对细胞分化抗原40(CD40)/细胞分化抗原40配体(CD40L)系统介导的内皮细胞激活的影响。方法采用人脐静脉内皮细胞株 ECV-304,CD40L 干预,使之与其表面的 CD40作用而使其激活,即血管细胞黏附分子-1(VCAM-1)的表达上调和淋巴细胞与内皮细胞黏附功能增强。再用不同浓度辛伐他汀或辛伐他汀(5μmol/L)+甲羟戊酸干预,流式细胞术和逆转录聚合酶链反应检测干预前后 VCAM-1的表达,流式细胞术检测 CD40L 介导的淋巴细胞与内皮细胞黏附功能。结果辛伐他汀可下调 CD40L介导的 VCAM-1的表达,并呈一定的剂量依赖性。甲羟戊酸(400μmol/L)抑制了辛伐他汀(5μmol/L)对 VCAM-1表达的下调作用。辛伐他汀可显著降低 CD40L 介导的淋巴细胞与内皮细胞的黏附功能。结论他汀类药物的抗炎作用与抑制 CD40/CD40L 系统有关,可能是通过抑制 HMG-CoA 还原酶而发挥作用的。
Objective To investigate the effects of simvastatin on vascular cell adhesion molecule-1 （VCAM-1） expression and adhesive function in ECV-304 cells treated with CD40L. Methods Human umbilical vein endothelial cell （HUVEC） was cultured and treated with various concentrations CD40L alone or in combination with various concentrations simvastatin in the absence or presence of mevalonic acid （400 μmol/L）. RT-PCR and FCM analysis were used to determine VCAM-1 expression and lymphocytes adhesion to endothelial cells. Results Simvastatin （0-10 μmol/L） decreased in a concentration-dependent manner the expression of VCAM-1 induced by CD40L and this effect could be blocked by cotreatment with mevalonic acid. Moreover, Simvastatin also significantly decreased adhesion capacity of lymphocytes to endothelial cells induced by CD40L. Conclusion Simvastatin downregulates VCAM-1 expression and adhesive capacity of lymphocytes to endothelial cells induced by CD40L.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
2007年第11期1046-1049,共4页
Chinese Journal of Cardiology
