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烟酸抑制血管紧张素Ⅱ诱导的内皮细胞C反应蛋白的表达 被引量:1

Niacin inhibits C-reactive protein expression induced by angiotensin Ⅱ in human endothelial cells
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摘要 目的探讨烟酸对血管紧张素Ⅱ诱导的人脐静脉内皮细胞(HUVECs)C反应蛋白表达的影响。方法分别使用不同浓度烟酸(0.25、0.5或1.0 mM)预处理HUVECs不同时间(1、2、6、12及24 h)后,使用血管紧张素Ⅱ(1μmol/L)诱导HUVECs表达C反应蛋白。荧光实时定量PCR(RT-PCR)检测CRP mRNA的变化。Western Blot检测CRP蛋白和NF-κB p65蛋白的变化。结果烟酸能抑制血管紧张素Ⅱ诱导的HUVECs中CRP mRNA和蛋白的表达,而且这种抑制呈时间和浓度依赖性。HUVECs在使用1 mmol/L烟酸预处理24 h后,AngⅡ+Niacin组与AngⅡ组相比,NF-κB蛋白表达有明显下降,同时CRP蛋白表达也同步下降。结论烟酸能抑制血管紧张素诱导的HUVECs中CRP mRNA及蛋白的表达,抑制NF-κB是可能的机制之一。 Objective To investigate the effect of niacin onC-reactive protein expression induced by angiotensinIIin human umbilical vein endothelial cells(HUVECs).Methods After HUVECswere pretreated with different concentrations of niacin(0.25,0.5,1.0 mM) for differenttime(1,2,6,12,24 h),HUVECs were treated with angiotensionⅡ(1 μmol/L) for 12 h.Realtime RT-PCR was used to detect changes of CRP mRNA level.Western blot analysis was used to detect changes of CRP and NF-κB p65 protein level.Results In HUVECs,Niacin inhibited C-reactive protein expression induced by angiotensinIIin time-and concentration-dependent way.The further study indicated that niacin has the ability to inhibited NF-κB p65 protein expression in HUVECs.Conclusion Niacin can decreaceC-reactive protein expression induced by angiotensinIIin HUVECs,and the possible mechanismis the inhabitation of NF-κB.
作者 张波 刘宏斌
出处 《中国医药导报》 CAS 2012年第13期170-172,共3页 China Medical Herald
关键词 内皮细胞 烟酸 C反应蛋白 血管紧张素Ⅱ NF-ΚB Endothelial cells Niacin AngiotensinII C-reaction protein NF-kappa B
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  • 1Meyers CD,Kamanna VS,Kashyap ML Niacin therapy in atherosclemsis [J]. Curr Opin Lipidol, 2004,15 : 659-65.
  • 2Kamanna VS,Kashyap ML. Nicotinic Acid (Niacin) Receptor Agonists: Will They Be Useful Therapeutic Agents? [J]. The American journal of cardiology, 2007,100 '. 53-61.
  • 3Holzhauser E,Albrecht C,Zhou Q,et al. Nicotinic acid has anti-athero- genic and anti-inflammatory properties on advanced atherosclerotic le- sions independent of its lipid-modifying capabilities [J]. J Cardiovasc Pharmacol, 2011,57:447-454.
  • 4Kaptoge S, Di AE ,L owe G,et al. C-reactive protein concentration and risk of coronary heart disease,stroke,and mortality:an individual par- ticipant meta-analysis [J]. Lancet,2010,375:132-140.
  • 5Bisoendial RJ,Boekholdt SM,Vergeer M,et al. C-reactive protein is a mediator of cardiovascular disease [J]. European Heart Journal,2010,31 : 2087-2091.
  • 6Kuvin JT,Dave DM,Sliney KA,et al. Effects of Extended-Release Niacin on Lipoprotein Particle Size,Distribution,and Inflammatory Markers in Patients With Coronary Artery Disease [J]. The American journal of car- diology, 2006,98 : 743-745.
  • 7Singh P, Hoffmann M ,Wolk R,et al. Leptin induces C-reactive protein expression in vascular endothelial cells [J]. Arterioscler Thromb Vasc Bio1,2007,27 : 302-307.
  • 8Yasojima K,Schwab C,Mcgeer EG,et al. Generation of C-reactive pro- tein and complement components in atherosclerotic plaques [J]. Am J Patho1,2001,158 : 1039-1051.
  • 9Mineo C, Gormley AK, Yuhanna IS, et al. Fc3,RIIB Mediates C-Reactive Protein Inhibition of Endothelial NO Synthase [J]. Circulation Research, 2005,97: 1124-1131.
  • 10Lira MY,Wang H,Kapoun AM,et al. p38 Inhibition attenuates the pro-inflammatory response to C-reactive protein by human peripheral blood mononuclear cells [J]. J Mol Cell Cardiol, 2004,37:1111-1114.

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