文章摘要
李伟,朱维维,殷寒秋.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[J].南京医科大学学报,2008,28(12):1569~1573
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
投稿时间:2008-06-10  
DOI:10.7655
中文关键词: 罗格列酮  人脐静脉内皮细胞  C反应蛋白  核因子κB
英文关键词: rosiglitazone  human umbilical vein endothelial cells  C reactive protein  nuclear factor kappa B
基金项目:徐州市科技局基金资助项目(X20052323)
作者单位
李伟 徐州医学院附属医院内分泌科,江苏 徐州〓221002 
朱维维  
殷寒秋  
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中文摘要:
      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)?CRP 5 μg/L组?CRP 20 μg/L组?CRP 100 μg/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?48 h 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100 μg/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?
英文摘要:
      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 cells(HUVECs),and explore the roles of rosiglitazone in the mechanism of anti-atherosclerosis. Methods:HUVECs cultured at the 5th 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.
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