期刊文献+

氢化可的松、辛伐他汀对高脂饮食大鼠动脉NF-ΚB、ICAM-1含量的影响 被引量:1

Experimental study of hydrocortisone and simrastatin on contout of NF-KB and ICAM-1 in the aorta of hypercholesterolemic rats
原文传递
导出
摘要 目的观察氢化可的松、辛伐他汀对高脂血症模型大鼠动脉核转录因子-KB(NF-ΚB)、血管细胞间粘附因子-1(ICAM-1)含量影响,探讨其防治动脉粥样硬化(AS)的机制。方法将普通级SD大鼠随机分为空白组、高脂组、氢化可的松组、辛伐他汀组。空白组喂以基础饲料,其余组喂以造模饲料并添加相应药物,16周后用放射免疫法检测血清中甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)含量;制作主动脉常规及免疫组化切片,观察内膜、肌层厚度及计算NF-KB、ICAM-1阳性细胞比率。结果氢化可的松、辛伐他汀组主动脉内膜及肌层厚度明显薄于高脂组、厚于空白组,其NF-KB、ICAM-1阳性细胞率显著低于高脂组、高于空白组。结论氢化可的松、辛伐他汀有抗AS作用,其机制可能通过抑制NF-KB激活和降低ICAM-1表达有关。 Objective To observe the effect of hydrocortisone,simvastatin on content of NF-KB and ICAM-1 in the aorta of hypercholesterolemic rats and to explore its mechanism in the preventment and treatment of the atherosclerosis.Methods Rats of common grade SD were divided into the blank group,the high fat diet group,hydrocortisone group,the Simvastatin group.The blank group was fed by baseline diet.The other groups were fed with the mold diet and drug.The experiment period was 16 weeks.After experiment,the TG,TC,LDL content in serum were determined using the radioimmunity method.By manufacture slice of the common and the immunohistochemistry,the thickness of the internal membrane and the muscular tunic were surveyed and the ratio of the positive cell of NF-KB p65 and ICAM-1 were calculated.Results The thickness of the aortic tunica intima and muscular tunic in the hydrocortisone group and the Simvastatin group were thinner than in the high fat diet group,and thicker than in the blank group.The ratio of the positive cell of NF-KB p65 and ICAM-1 in the hydrocortisone group and the Simvastatin group were less than in the high fat diet group,and larger than in the blank group.Conclusion The Hydrocortisone and Simvastatin can reduce secretion of both NF-KB and ICAM-1,which may thereby influence the pathogenesis of atherosclerosis.
出处 《临床医学》 CAS 2008年第7期106-108,F0004,共4页 Clinical Medicine
关键词 动脉粥样硬化 核转录因子-KB 血管细胞间粘附因子-1 氢化可的松 辛伐他汀 大鼠 Atherosclerosis NF-KB ICAM-1 Hydrocortisone Simvastatin Rat
  • 相关文献

参考文献12

  • 1Ross R. Atherosclerosis is an inflammatory disease[ J]. Am Heart J, 1999,138:419 - 20.
  • 2Ibragimov Al, McNeal C J, Ritter LR, et al. A mathematical model of atherogenesis as an inflammatory response [ J ]. Math Med Biol,2005, 22(4) :305 -33.
  • 3Kanters E, Gijbels MJ, Vergouwe MN, et al. Hematopoietic NF - kB1 deficiegcy results in small atherosclerotic lesions with an inflammatory phenotype [ J ]. Blood,2004,103 ( 3 ) :934 - 40.
  • 4Gaugler MH,Vereycken - Holler V,Squiban C ,et al. Pravastatin limits endothelial activation after irradiation and decreases the resulting inflammatory and thrombotic, responses [ J. Radiat Res,2005,163 (5) :479 - 87.
  • 5Li D, Chen H, Romeo F,et al. Statins modulate oxidized low - density lipoprotein- mediated adhesion molecule expression in human coronary artery, endothelial cells: role of LOX - 1 [ J]. J Pharmacol Exp Ther,2002,302(2) :601 -5.
  • 6Nachtigal P, Pospisilova N,Pospechova K,et al. MDOC and atorvastatin have potential antiinflammatory effects in vascular endothelium of apoE - / - mouse model of atherosclerosis [ J ]. Life Sci, 2006,78 (17):1 983-9.
  • 7Lu Y.Fukuda K,Nakamura Y,et al. Inhibitory effect of triptolide on chemokine expression induced by proinflammatory cytokines in human corneal fibroblasts. Invest Ophthalmol Vis Sci,2005,46(7) :2 346 -52.
  • 8Johns DG,Ao Z,Willette RN,et al. Role of p38 MAP kinase in post- capillary venule leukocyte adhesion induced by ischemia/reperfusion injury [ J ]. Pharmacol Res,2005,51 (5) :463 - 71.
  • 9Bolick DT, Srinivasan S, Whetzel A, et al. Lipoxygenase Mediates Monocyte Adhesion to Aortic Endothelium in Apolipoprotein E - Deficient Mice Through Activation of RhoA and NF - { kappa } B[ J]. Arterioscler Thromb Vasc Biol,2006: 16.
  • 10Ahn KS,Aggarwal BB. Transcription Factor NF - { kappa } B: A Sensor for Smoke and Stress Signals [ J]. Ann N Y Aead Sci,2005,1056: 218 -33.

同被引文献13

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部