罗格列酮对C反应蛋白作用下人脐静脉内皮细胞生长、凋亡及核因子κB表达的影响

Effect of rosiglitazone on C reactive protein induced growth,apoptosis and the expression of nuclear factor kappa B in human umbilical vein endothelial cells

目的:研究C反应蛋白(CRP)作用下人脐静脉内皮细胞(HUVECs)的生长、凋亡及核因子κB(NF-κB)表达情况以及罗格列酮(RSG)干预对其的影响,以探讨CRP在抗动脉粥样硬化(AS)中的作用。方法:体外培养HUVECs,细胞传至第5代,随机分为8组:正常对照组(NG)、CRP5μg/L组、CRP20μg/L组、CRP100μg/L组、罗格列酮对照组(RSG组)、RSG+CRP5组、RSG+CRP20组、RSG+CRP100组,分别检测CRP作用下和RSG干预后12、24、48h HUVECs的生长、凋亡及NF-κB表达情况。结果:CRP各质量浓度组HUVECs的凋亡及NF-κB的表达明显高于NG(P<0.05),生长低于NG,尤以100μg/L浓度时更明显(P<0.05)。RSG干预后HUVECs的凋亡及NF-κB的表达明显低于其相应对照组(P<0.05),生长高于其相应对照组,并随时间的延长而更加明显。结论:CRP可促进HUVECs凋亡,抑制其生长,诱导NF-κB表达增加,提示CRP能激活炎症反应,在AS的病理机制中发挥重要作用。RSG能有效降低CRP的致炎症效应有助于延缓糖尿病AS的进程。

Objective：To investigate the effect of rosiglitazone（RSG）on C reactive protein（CRP） induced growth,apoptosis and the expression of nuclear factor kappa B（NF-κB） in human umbilical vein endothelial celIs（HUVECs）,and explore the roles of rosiglitazone in the mechanism Of anti-atherosclerosis. Methods：HUVECs cultured at the 5^th generation were divided into eight groups：Normal control group（NG）,CRP 5 μg/L group（CRP 5）,CRP 20 μg/L group（CRP 20）,CRP 100 μg/L group（CRP 100）,RSG control group （RSG）,RSG and CRP 5 group,RSG and CRP 20 group,RSG and CRP 100 group. Cells were intervened by RSG （5 μmoL/L） for 12,24 and 48 hours. RT-PCR was used to detect the expression of NF-κB. The growth and apoptosis of HUVECs were also observed. Results：The expression of NF-κB and the apoptosis were obviously higher in the each mass concentration CRP group than that in the NG （P 〈 0.05）, more obviously when the concentration was 100 μg/L （P 〈 0.05）,and the growth change was opposite. The mRNA expression level of NF-κB and the apoptosis in cells treated by RSG were lower significantly than that of control group （P 〈 0.05）, the growth was higher than that of control group, and it was significantly higher with the increase of the time. Conclusion： CRP promoted the apoptosis and inhibited the growth of Certain density CRP can induce the expression of NF-κB,which indicated that CRP can activate the inflammation response, and play a vital role in the pathology mechanism at coronal AS. Rosiglitazone can effectively reduce the inflammation effect of CRP thus to delay the occurrence of the AS.