摘要
目的研究氧化低密度脂蛋白(ox-LDL)对人脐静脉内皮细胞表达分化抗原CD40中核因子κB(NF-κB)的作用,进一步探讨卡托普利可能的抗动脉硬化作用。方法在ox-LDL作用人脐静脉内皮细胞前预先用卡托普利、NF-κB阻断剂(PDTC)、卡托普利+一氧化氮合酶阻断剂(L-NAME)、卡托普利+PDTC作用后,应用流式细胞技术检测细胞表面CD40的表达。结果预先加入卡托普利、PDTC人脐静脉内皮细胞的CD40的表达低于ox-LDL组(P<0.05),卡托普利组内皮细胞CD40的表达值低于卡托普利+PDTC组和卡托普利+NAME组,组间相比差异显著(P<0.001)。结论ox-LDL通过NF-κB途径激活了CD40的表达,卡托普利通过一氧化氮(NO)途径及NF-κB的转录使ox-LDL引起的内皮细胞CD40的表达下降,从而具有抗动脉硬化作用。
Objective To investigate the action of NF-κB in oxidized low-density lipoprotein induced the expression of CD40 in cultured human umbilical vein endothelial cells, and the anti-atherosclerosis action of captopril. Methods HUVECs was incubated in vitro. PDTC(NF-κB inhibitor), captopril, captopril + L-NAME (nitric oxide synthase blockade), captopril+ PDTC were co-incubated with HUVECs for lh before ox-LDL were co-incubated with HUVECs for 24h . The expression of CD40 was measured by flow cytometric analysis. Results The expressions of CD40 in PDTC, captopril groups were under ox-LDL groups(P(0.051, The expression of CD40 in captopril group was under captopril + L-NAME, captopril+ PDTC groups(P(0. 001). Conclusions Ox-LDL induced the expression of CD40 via NF-κB; Captopril can partially inhibit the high expression of CD40 on HUVECs induced by ox-LDL through NO and NF-κB, that maybe the mechanism of the anti-atherosclerosis action of captopril.
出处
《中国心血管杂志》
2005年第4期258-259,298,共3页
Chinese Journal of Cardiovascular Medicine