期刊文献+

氢化可的松与辛伐他汀对高脂饮食大鼠动脉NF-κB与ICAM-1含量的影响 被引量:2

The Effect of Hydrocortisone and Simvastatin on Contents of NF-κB and ICAM-1 in Aorta of Hypercholesterolemic Rats
下载PDF
导出
摘要 目的观察氢化可的松与辛伐他汀对高脂血症模型大鼠动脉核转录因子-κB(NF-κB)、血管细胞间粘附因子-1(ICAM-1)含量的影响,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,氢化可的松高、低剂量组和辛伐他汀组。空白组饲喂基础饲料,其他组饲喂造模饲料并给予相应药物,16周后采用放射免疫法检测血清中三酰甘油(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NF-κB、ICAM-1阳性细胞比例。结果氢化可的松高、低剂量组,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-κB、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-κB激活和降低ICAM-1分泌有关。 Objective To investigate the effect of hydrocortisone, simvastatin on contents of NF-kB and ICAM-1 in the aorta of hypercholesterolemie rats and its mechanism of preventing and treating atherosclerosis. Methods SD rats were divided into the blank group, high-fat diet group, hydrocortisone group, and simvastatin group. Rats in the blank group were fed with normal diet. Rats in other groups were fed with lipid-rich diet and drugs. 16 weeks later, contents of TG, TC, LDL in serum were detected by the radioimmunity method. The internal membrane, muscular layer and ratio of positive cells with NF-kB p65 and ICAM-1 were observed by immunohistochemistry technique. Results The aortic tunica intima and muscular layer in hydrocortisone group and simvastatin group were thicker than those in the high-fat diet-fed group, but thinner than those in the blank group. The ratio of the positive cell of NF-kB p65 and ICAM-1 in hydrocortisone group and simvastatin group were less than in high-fat diet group, and larger than those in the blank. Conclusion Both hydrocortisone and simvastatin have antiatherosclerosis effects, which could be attributed to inhibited activation of NF-KB and secretion of ICAM-1.
出处 《医药导报》 CAS 2008年第11期1320-1323,共4页 Herald of Medicine
关键词 氢化可的松 辛伐他汀 动脉粥样硬化 核转录因子-KB 血管细胞间粘附因子-1 Hydrocortisone Simvastatin Atherosclerosis NF-kB ICAM-1
  • 相关文献

参考文献12

  • 1ROSS R . Atherosclerosis is an inflammatory disease [ J ]. Am Heart J,1999,138(5 Pt 2) :S419 -420.
  • 2IBRAGIMOV A I, MCNEAL C J, RITTER L R, et al. A mathematical model of atherogenesis as an inflammatory response[J]. Math Med Biol, 2005,22 ( 4 ) :305 - 333.
  • 3KANTERS E, GIJBELS M J, VAN-DER M,et al. Hema-NF-kappaB1 deficiency resuhsin small atherosclerotic lesions with an inflammatory phenotype[J].Blood,2004,103 (3) :934 - 940.
  • 4GAUGLER M H, 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 - 487.
  • 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 - 605.
  • 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) :1983 - 1989.
  • 7LU Y, FUKUDA K, NAKAMURA Y,et al. Inhibitory effect of triptolide on chemokine expression induced by proinflammatory cytokines in human corneal fibroblasts[J]. Invest Ophthalmol Vis Sci, 2005,46 ( 7 ) : 2346 - 2352.
  • 8JOHNS D G, AO Z, WILLETTE R N,et al. Role of p38 MAP kinase in postcapillary venule leukocyte adhesion induced by ischemia/reperfusion injury[J]. Pharmacol Res ,2005,51 (5) :463 -471.
  • 9BOLICK D T, 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,2006,26 : 1260 - 1262.
  • 10AHN K S, AGGARWAL B B. Transcription factor NF- │kappa │ B : a sensor for smoke and stress signals[J].Ann N Y Acad Sci ,2005,1056:218 - 233.

同被引文献24

  • 1向自军.妇科千金片治疗慢性盆腔炎102例[J].湖北中医杂志,2007,29(8):41-41. 被引量:11
  • 2Yamamoto Y, Gaynor RB. IkappaB kinases: key regulators of the NF- kappat3 pathway [J].Trends Biochem. Sci, 2004, 29(2) : 72- 79.
  • 3Jawien J, Gajda M, Mateuszuk L, et al. Inhibition of Nuclear factor- kB attenuates atherosclerosis in apoE/ LDLR- Double knockout mice [ J ]. Physiol Pharmacol, 2005, 56(3) : 483- 489.
  • 4Brasier AR. The NF - kappaB regulatory network [J ]. Cardiovase Toxicol, 2016 , 6 (2) : 111.
  • 5Orr AW, Hahn C, Blackman I3R, et al. PAK signaling regulates oxidant- dependent NF KB activation by flow [J]. Circ Res, 2008,103(6): 671 - 679.
  • 6Gregorio Brevetti, Vittorio Schiano, Massimo Chiariello. Cellular adhesion molecules and peripheral arterial disease [J ]. Vascular Medicine, 2006,11 : 39 - 47.
  • 7YunBiao Lu, LarryM Wahl. Production of matrix metalloproteinase- 9 by activated human monocytes involves a phosphatidylinositol - 3 kinase/Akt/iKKa/NF -kB pathway [J]. Journal of Leukocyte Biology, 2005,78:259 - 265.
  • 8Brasier AR. The nuclear factor- kappaB- interleukin - 6 signalling pathway mediating vascular inflammation [J ]. Cardiovasc Res, 2010,86(2) :211 - 218.
  • 9Li Na,Cao Shu- hua. Research Progression of NF- kB in inflammatory and immune reaction of organism [ J ]. Chin J Emerg Med, 2007,16 ( 14 ) : 442 - 444.
  • 10Geethalakshmi Radhakrishnan, Ryoko Suzuki, Hironori Maeda, et al. Inhibition of Neointimal Hyperplasia Development by MC1 - 186 is Correlated With Downregulatin of Nuclear Factor- kB Pathway [J ]. Cite J, 2008, 72:800- 806.

引证文献2

二级引证文献16

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