期刊文献+

维生素E对糖尿病大鼠高级糖基化终末产物及其受体和肾功的影响 被引量:3

Effect of Vitamin E on advanced glycosylation end-products and their receptors in renal tissue of diabetic rats
下载PDF
导出
摘要 目的观察维生素E对糖尿病大鼠高级糖基化终末产物(AGEs)及其受体(RAGE)和肾功能的影响。方法利用链脲佐菌素腹腔注射法诱导建立糖尿病大鼠模型。将实验用SD大鼠随机分为正常对照组(NC组)、糖尿病组(DM组)和维生素E治疗组(VE组),治疗8周。观察大鼠的一般状况,监测血糖(BGL)、糖化血红蛋白(HbA1C)、尿素氮(BUN)、血肌酐(Scr)、内生肌酐清除率(Ccr)、尿白蛋白排泄率(UAER)、肾重/体重比值;应用荧光显微镜观察肾脏组织AGEs,免疫组化方法检测RAGE含量。结果①与NC组比较,DM组大鼠体重、血糖、HbA1C、BUN、UAER、肾重/体重比值均明显增高(P<0.01),Ccr明显下降(P<0.01),肾脏AGEs及RAGE含量均明显增高(P<0.01);②与DM组相比,VE组UAER、肾重/体重比值明显降低(P<0.05),Ccr明显升高(P<0.01),肾脏AGEs及RAGE含量均明显降低(P<0.05)。结论维生素E无降糖作用,但可能通过减轻糖尿病大鼠肾组织的非酶糖基化过程,从而减轻AGEs与受体结合后导致的对肾脏组织的损伤,对糖尿病大鼠肾脏具有保护作用。 Objective To observe the effect of Vitamin E on advanced glycosylation end-products (AGEs) and their receptors in renal tissue of diabetic rats. Methods Rat diabetic nephropathy was induced by intraperitoneal injection of STZ. Rats were allocated to normal control group (NC group), diabetes mellitus group (DM group), and Vitamin E group (VE group). All rats were treated with corresponding drugs for 8 weeks. During and after the treatment, the general state, blood glucose level (BGL), blood urea nitrogen (BUN), serum creatinine (Scr), urinary albumin excretion rate (UAER), glycosylated hemoglobin (HbA1C), clearance rate of creatinine (Ccr) and kidney weight/body weight ratio were determined in different groups. The fluorescence microscope was used to observe advanced glycosylation end-products fluorescence intensity in iced slices. The expression of RAGE in rats' renal tissue slices was measured by immunohistochemistry. Results (1) Compared with those in NC group, GLU, HbA1C, BUN, UAER, kidney weight/body weight ratio, contents of AGEs, and RAGE increased significantly (P〈0.01), while Ccr decreased significantly ( P 〈 0.01) in DM group. (2) Compared with those in DM group, UAER, kidney weight/body weight ratio, contents of AGEs, and RAGE decreased significantly (P〈0.05), while Ccr significantly (P〈0.05) increased in VE group. Conclusion Vitamin E has no effect in decreasing blood glucose level, but has a certain role in preventing renal function by alleviating the accumulation of advanced glycosylation end-products.
出处 《西安交通大学学报(医学版)》 CAS CSCD 北大核心 2008年第3期297-300,共4页 Journal of Xi’an Jiaotong University(Medical Sciences)
关键词 高级糖基化终末产物 高级糖基化终末产物受体 维生素E 糖尿病肾病 advanced glycosylation end-products (AGEs) receptor for advanced glycation end-products(RAGE) Vitamin E diabetic nephropathy
  • 相关文献

参考文献10

  • 1Martin B, Sybille F, Gunter W, et al. The advanced glycation end product N (epsilon)-carboxymethyllysine is not a predictor of cardiovascular events and renal outcomes in patients type 2 diabetic kidney disease and hypertension [J]. Am J Kidney Dis, 2006, 48(4) :571-579.
  • 2Koya D, Lee IK, Ishii H, et al.. Prevention of glomerular dysfunctions in diabetic rats by treatment of d-a -tocopherol [J]. Am Soc Nephrol, 1997, 8:426-435.
  • 3Hammes H, Martin S, Federlin K, et al. Aminoguanidine treatment inhibits the development of experimental diabetic retinopathy [J]. Proc Natl Acad Sci USA, 1991, 88:11555-11558.
  • 4Goldin A, Beckman JA, Schmidt AM, et al. Advanced glycation end products: Sparking the development of diabetic vascular injury [J]. Circulation, 2006, 114:597-605.
  • 5Suzuki D, Toyoda M, Yamamoto N, et al. Relationship between the expression of advanced glycation end-products (AGE) and the receptor for AGE (RAGE) mRNA in diabetic nephropathy[J]. Clin Invest, 2006, 45(7) :435-441.
  • 6Yasuhiko Y , Ichiro K, Toshio D, et al. Development and prevention of advanced diabetic nephropathy in RAGE-overexpressingmice [J]. J Clin Invest, 2001, 108(2):261-268.
  • 7Wendt TM, Tanji N, Guo J, et al. RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy [J]. Am J Pathol, 2003, 162(4) :1123-1137.
  • 8Wautier MP, Chappey O, Corda S, et al. Activation of NADPH oxidase by AGE links oxidant stress to altered gene expression via RAGE [J]. Am J Physiol Endocrinol Metab, 2001, 280 (5) :685-694.
  • 9Brownlee M. The pathobiology of diabetic complications: a unifying mechanism [J]. Diabetes, 2005, 54 : 1615-1625.
  • 10Du XL, Edelstein D, Rossetti L, et al. Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathyway and induces plasminogen activator inhibitor-1 expression by increasing spl glycosylation [J]. Proc Natl Acad Sci USA, 2000, (97) :12222-12226.

同被引文献38

  • 1陈澍,刘雪芳.链脲佐菌素诱导大鼠糖尿病肾病模型的建立[J].实用医学杂志,2006,22(11):1239-1240. 被引量:33
  • 2袁继丽,刘成海,姜哲浩,张悦,刘成.口服氯化汞对大鼠肾间质纤维化的作用[J].中国实验动物学报,2006,14(2):93-95. 被引量:10
  • 3Mofensen CE,Keane WF,Benntt PH,et al.Prevention of diabetic renal disease with special reference to microalbuminuria[J].Lancet,1995,346(3983):1080-1084.
  • 4Ghosh A,Sil PC.A protein from Ca janus indicus Spreng protects liver and kidney against mercuric chlorideinduced oxidative stress.Biol Pharm Bull.2008; 31(9):1651-1658.
  • 5Vahter M,Akesson A,Lind B,Bj(o)rs U,Schütz A,Berglund M.Longitudinal study of methylmercury and inorganic mercury in blood and urine of pregnant and lactating women,as well as in umbilical cord blood.Environ Res.2000; 84(2):186-194.
  • 6Richer G,Ducrot H,Hamburger J,Legrain M,Maxwell M,Péquignot MH.May medical therapy of arterial hypertension by used in patients with renal failure?Presse Med.1968; 76(44):2103-2106.French.
  • 7Liu Y.Epithelial to mesenchymal transition in renal fibrogenesis:pathologic significance,molecular mechanism,and therapeutic intervention.J Am Soc Nephrol.2004; 16(1):1-12.
  • 8Nielsen JB,Andersen O.Oral mercuric chloride exposure in mice:effects of dose on intestinal absorption and relative organ distribution.Toxicology.1989 ; 59(1):1-10.
  • 9Nielsen JB,Andersen O.Disposition and retention of mercuric chloride in mice after oral and parenteral administration.J Toxicol Environ Health.1990; 30(3):167-180.
  • 10Coates ME,Kon SK,Porter JW.Vitamins in animal nutrition.Br Med Bull.1956; 12(1):61-66.

引证文献3

二级引证文献10

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