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缬沙坦对兔高脂血症肾脏的保护作用 被引量:1

Renoprotective Effects of Valsartan in Rats with Hyperlipemia
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摘要 目的:观察兔高脂血症肾组织血管紧张素Ⅱ(AngⅡ)、核转录因子κB(NF-κB)、血管细胞黏附分子-1(VCAM-1)和碱性成纤维细胞生长因子(bFGF)的表达以及缬沙坦的干预作用。方法:24只健康雄性新西兰白兔随机分为3组,每组8只,正常对照组(A组)、高脂饮食组(B组)和治疗组(C组)。10周后,测定血清总胆固醇(TC)、三酰甘油(TG)和低密度脂蛋白(LDL)的浓度;HE染色观察肾组织病理改变,并用免疫组化方法测定AngⅡ、NF-κB、VCAM-1和bFGF的表达。结果:高脂血症时,肾组织同NF-κB、VCAM-1和bFGF表达增强;高脂饮食组相比,治疗组NF-κB、VCAM-1和bFGF在肾组织中的表达明显降低(P<0.05)。缬沙坦降低NF-κB、VCAM-1和bFGF在肾组织中的表达,减轻肾组织的炎症反应,抑制肾组织纤维化。结论:缬沙坦对兔高脂血症肾脏可能具有保护作用。 Objective: To observe the expression of angiotensin Ⅱ (Ang Ⅱ ), nuclear factor-κB (NF-κB) ,vascular cell adhesion molecule 1 (VCAM-1) ,basic fibroblast growth factor (bFGF) and the intervention of valsartan. Methods: A total of 24 healthy male New Zealand white rabbits were randomly divided into three groups. They were a normal control group (group A ), an atherogenic diet group( group B) and a treatment group( group C) (n = 8 in each group). The concentrations of serum total cholesterol (TC), triglyceride (TG) and low density lipoprotein (LDL) were detected by BackmaanLX20 automatic biochemical analyzer after ten weeks. Renal histopathological changes were observed by HE stain and the expression of Ang Ⅱ , NF-κB, VCAM-1 and bFGF was determined by immunohistochemistry. Results: There was a strong expression of renal tissues and NF-κB, VCAM-1 and bFGF in hyperlipedmia. Compared with the atherogenic diet group, the expression of NF-κB, VCAM-1 and bFGF in renal tissues of the treatment group decreased significantly (P 〈0.05). Valsartan could reduce the expression of NF-κB, VCAM-1 and bFGF in renal tissues, relieve inflammatory response of renal tissues and inhibit renal fibrosis. Conclusion:Valsartan may have protective effects for renes of rats with hyperlipemia.
出处 《山西职工医学院学报》 CAS 2008年第2期11-13,共3页 Journal of Shanxi Medical College for Continuing Education
关键词 缬沙坦 高脂血症 valsartan ren hyperlipemia
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  • 1Gibbons GH. The pathophysiology of hypertension : the importance of angiotensin Ⅱ in cardiovascular remodeling [ J ]. Am J Hypertens, 1998,11(11 Pt2) :177S-181S.
  • 2Inagami T. Renin in the brain and neuroblastoma cells : an endogenous and intracellular system [ J ]. Neuroendocrinology, 1982,35 ( 6 ) : 475- 482.
  • 3Dzau VJ. Theodore Cooper Lecture: Tissue angiotensin and pathobiology of vascular disease: a unifying hypothesis [ J ]. Hypertension, 2001,37(4) :1047-1052.
  • 4Eddy AA. Molecular basis of renal fibrosis [ J ]. Pediatr Nephrol,2000, 15(3-4) :290-301.
  • 5Porcile C, Piccioli P, Stanzione S ,et al. Proteasome inhibitors induce cerebellar granule cell death : inhibition of nuclear factor-κB activation [J]. Ann N Y Acad Sci ,2002,973:402-413.
  • 6Omori M, Ogino T, Than TA,et al. Monochloramine inhibits the expression of E-selectin and intercellular adhesion molecule-1 induced by TNF-alpha through the suppression of NF-kappaB activation in human endothelial cells[J]. Free Radic Res,2002,36(8) :845-852.
  • 7Chuluyan HE, Osborn L, Lobb R,et al. Domains 1 and 4 of vascular cell adhesion molecule-1 (CD106) both support very late activation antigen-4 (CD49d/CD29)-dependent monocyte transendothelial migration[ J]. J Immunol,1995,155(6) :3135-3145.
  • 8Brennan DC, Jevnikar AM, Takei F, et al. Mesangial cell accessory functions: mediation by intercellular adhesion molecule-1 [J]. Kidney Int, 1990,38 (6) : 1039-1046.
  • 9Wuthrich RP. Intercellular adhesion molecules and vascular cell adhesion molecule-1 and the kidney[ J ]. J Am Soc Nephrol, 1992,3 (6) : 1201-1211.
  • 10Timoshanko JR, Sedgwick JD, Holdsworth SR,et al. Intrinsic renal ceils are the major source of tumor necrosis factor contributing to renal injury in murine crescentic glomerulonephritis [ J ]. J Am Soc Nephrol,2003,14(7 ) : 1785-1793.

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