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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 effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase on the differentiation of human CD40 / CD40L in human umbilical vein endothelial cells The effect of endothelial cell activation. Methods The human umbilical vein endothelial cell line ECV-304 and CD40L were intervened to make them activated by CD40 on the surface, namely, the up-regulation of the expression of vascular cell adhesion molecule-1 (VCAM-1) and the adhesion of lymphocytes to endothelial cells Enhanced. The expression of VCAM-1 was detected by flow cytometry and reverse transcription-polymerase chain reaction (RT-PCR) before and after intervention with different concentrations of simvastatin or simvastatin (5μmol / L) plus mevalonate. Flow cytometry was used to detect the expression of CD40L Lead lymphocytes and endothelial cell adhesion function. Results Simvastatin could down-regulate CD40L-mediated VCAM-1 expression in a dose-dependent manner. Mevalonate (400 μmol / L) inhibited the down-regulation of VCAM-1 expression by simvastatin (5 μmol / L). Simvastatin can significantly reduce CD40L-mediated adhesion of lymphocytes and endothelial cells. Conclusion The anti-inflammatory effect of statins is related to the inhibition of CD40 / CD40L system and may play a role by inhibiting HMG-CoA reductase.