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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。
AIM: To investigate the effects of C-reactive protein (CRP) on the growth, apoptosis and the expression of NF-κB in human umbilical vein endothelial cells (HUVECs) and the effects of rosiglitazone (RSG) To investigate the role of CRP in anti-atherosclerosis (AS). Methods: HUVECs were cultured in vitro. The cells were passaged into passage 5 and randomly divided into 8 groups: normal control group (NG), CRP5μg / L group, CRP20μg / L group, CRP100μg / L group, rosiglitazone control group ), RSG + CRP5 group, RSG + CRP20 group and RSG + CRP100 group. The growth, apoptosis and NF-κB expression of HUVECs were detected by CRP and 12, 24 and 48 h after RSG intervention. Results: The apoptosis and the expression of NF-κB in HUVECs were significantly higher than those in NG (P <0.05). The growth was lower than NG, especially in the concentration of 100μg / L (P <0.05). The apoptosis of HUVECs and the expression of NF-κB in RSV-treated HUVECs were significantly lower than those in the corresponding control group (P <0.05), and were higher than those in the corresponding control group and were more obvious with the prolongation of time. CONCLUSION: CRP can promote apoptosis of HUVECs, inhibit its growth and induce an increase of NF-κB expression, suggesting that CRP can activate inflammatory reaction and play an important role in the pathogenesis of AS. RSG can effectively reduce the inflammatory effects of CRP can help delay the progression of diabetic AS.