期刊文献+

黄芪对糖尿病大鼠肾组织NF-κB和MCP-1表达的影响 被引量:13

Effect of Astragalus on expression of NF-kB and MCP-1 in renal tissues of diabetic Rats
在线阅读 下载PDF
导出
摘要 目的研究(NF-κB)和(MCP-1)在糖尿病肾病(DN)大鼠肾组织中的变化并探讨黄芪对NF-κB和MCP-1表达的影响及其对糖尿病大鼠肾脏的保护作用。方法将大鼠随机分成正常对照组(C组)、糖尿病组(DM组)、糖尿病黄芪组(DT组);生化法测定血肌酐及24h尿蛋白;免疫组织化学法检测各组大鼠肾组织NF-κB、MCP-1的表达。结果C组肾小球NF-κB及MCP-1在有少量表达,DT组肾小球中NF-κB、MCP-1表达较DM组有下降(P<0.05);DM组血肌酐和24h尿蛋白较C组升高(P<0.01),而DT组较DM组明显降低(P<0.05);DT组较DM组病理学损害有改善。结论黄芪能减少尿蛋白、延缓肾功能进展、改善肾组织病理学损害,对糖尿病肾病大鼠有治疗作用,其机制之一可能是通过抑制NF-κB的活化和MCP-1表达而实现的。 Objective To investigate the changes of nuclear factor kappaB (NF-κB) and Monocyto Chemoatractant Protein-1 (MCP-1) in renal tissues of diabetic rat and the protective function of astragalus in diabetic rats. Methods SD male rats were randomly divided into three groups which were normal control group (C), diabetic group (DM), and astragalus treated group (DT). The expressions of NF-κB and MCP-1 were measured by Immuno-histochemstry. The levels of creatinine (Cr) and 24- hour urine protein excretion were measured by Biochemistry. Results Immunohistochemstry revealed that the expression of NF-κB and MCP-1 in glomeruli significantly increased in DM group (P〈0. 01) and the expression of them in DT group more decreased than that in DM group (P〈0. 05). The levels of 24-hour urine protein and Cr in DM group were higher than those in DT group (P〈0. 05). Compared with DM group, examination of kidney sections in DT group rats showed that renal histology changes including mesangium expansion, proliferation of mesangial cells, infiltration of mononuclear cells and extraeellular matrix accumulation were markedly improved. Conclusion These results suggest that the activated NF-κB and expression of MCP-1 plays an pathogenic role in the development of diabetic nephropathy. Astragalus can reduce urine protein excretion, improve renal function, ameliorated renal histology changes and halt progression of diabetic nephropathy. The mechanism perhaps was related to the reduction NF-κB and MCP-1 expression in renal tissues in diabetic rats.
出处 《贵州医药》 CAS 2009年第2期102-105,共4页 Guizhou Medical Journal
关键词 糖尿病肾病 核因子-ΚB 单核细胞趋化蛋白-1 黄芪 Diabetic nephropathy NF-κB MCP-1 Astragalus
  • 相关文献

参考文献14

  • 1刘志红,黎磊石.糖尿病肾病发病机理[J].中华肾脏病杂志,1999,15(2):120-123. 被引量:314
  • 2Morrissey J, Kiahr S. Transcription factor NF-kappa B regulation of renal fibrosis during ureteral obstruction [J]. NephrL, 1998,18(6) : 603-611.
  • 3Kumat A, Rlawkins KS, Hannan MA, et al. Activation of PKC-BATA(Din glomerular mesang ial cell is associated with specific NF-kappa B subunit translocation [J]. Am J Physiol Renal Phys iol, 2001,281: F613-616.
  • 4Quehenberger P, Biehaus A, Fasching P, et al. Endothelin 1 transcr-iption is controlled by nuclear factorkappa B in AGE-stimulatedcultured endotheliaL cells [J]. Diabetes, 2000,49 : 1561-1570.
  • 5Ruiz-ortega M, Bustos C, Hernandez-presa MA, et al. Angiotensin Ⅱ participates in mononuclear cell recruitment in experimental immune complex nephritis through nuclear factor kappa B activation and monocyte chemoattractant protein-1 synthesis[J]. J Immunol, 1998,161:430-439.
  • 6徐郁杰,张庆怡,吴青伟.黄芪对糖尿病大鼠早期肾肥大和蛋白尿的影响[J].上海第二医科大学学报,1997,17(5):357-359. 被引量:117
  • 7于德民,吴锐,尹潍,袁咏.实验性链脲佐菌素糖尿病动物模型的研究[J].中国糖尿病杂志,1995,3(2):105-109. 被引量:425
  • 8Siebealist U, Frananro G, Brow K, et al. Structure, regulation and functio of NF-κB[J]. Annu Rev Biol, 1994, 10:405-455.
  • 9Alerts,Balclwin TR. The NF-κB and IB protein, new discoveries and insights[J]. Annu Rev Immunl, 1996, 14 : 649-681.
  • 10Donadalli R, Abbate M, Zanchic, et al. Protein traffic activates NF-κB genes signaling and promotes MCP- 1-dependent interstitial inflammation [J]. Am J Kindey Dis,2000,36(60):1226-1241.

二级参考文献10

  • 1朴忠浩,中国糖尿病杂志,1996年,4期,31页
  • 2韩晓亮,中华肾脏病杂志,1989年,5卷,134页
  • 3Wang YP,Li XY,Song CQ, et al. Effect of of astragaloside Ⅳ on T,B lymphocyte proliferation and peritoneal macrophages function in mice. Acta Pharmacol Sin,2002,23: 263
  • 4Takada M, Nadeau KC, Shaw GD, et al. Prevention of late renal changes after initial ischemia/reperfusion injury by blocking early selectin binding. Transplantation, 1997,64:1520
  • 5Jain S,Bicknell G R,Nicholson ML. Molecular changes in extracellular matrix turnover after renal ischaemia-reperfusion injury. Br J Surg ,2000,87 :1188
  • 6Forbes JM, Hewitson TD, Becker GJ, et al. Ischemic acute renal failure:long-term histology of cell and matrix changes in the rat.Kidney Int ,2000,57:2375
  • 7Rnggenenti P, Perna A, Mosconi L, et al. Urinary protein excretion rate is the best independent predictor of ESRF in non-diabetic proteinuric chronic nephropathies. Kidney Int, 1998,53:1209
  • 8Bruijn JA, de Heer E. Adhesion molecules in renal diseases. Lab Invest., 1995,72: 387
  • 9Tang WW, Qi M,Warren JS, et al. Chemokine expression in experimental tubulointerstitial nephritis. J Immunol, 1997,159:870
  • 10Sung FL,Zhu TY,Kathy KW, et al. Enhanced MCP-1 expression during ischemia/reperfusion injury is mediated by oxidative stress and NF-KB. Kidney Int ,2002,62:1160

共引文献862

同被引文献207

引证文献13

二级引证文献101

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