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激活素A及卵泡抑素基因在糖尿病大鼠肾脏表达的实验研究 被引量:1

Experimental Research of Activin A and Follistatin Gene Expression in the Kidney of Diabetic Rats
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摘要 目的:探讨激活素A(ACT-A)及卵泡抑素(FS)基因在糖尿病大鼠肾脏的表达及可能机制。方法:雄性Wistar大鼠,随机分成对照组(NC)和糖尿病组(DM),腹腔注射STZ诱导糖尿病模型。各组分别在术后4、8、12和16周处死6只大鼠。观察各组肾重/体重(KW/BW)、24h尿白蛋白排泄率(AER)及肌酐清除率(Ccr)的变化。real time-PCR检测各组肾组织ACT-A及FS基因的表达。结果:与NC组相比,DM组大鼠从第8周末开始KW/BW、AER及Ccr均显著上升(P<0.01),16周末时达峰值。DM组大鼠从第4周末开始ACT-A mRNA表达逐渐增加,第12周末时达峰值(P<0.01)。FS mRNA在NC组各时间点大鼠肾组织大量表达,而在DM组其表达量呈逐渐下降趋势,第16周时只能检测到基础量表达。结论:ACT-A及FS表达失衡在DN的进行性发展中发挥了重要作用。 Objective:To explore the effect of activin A and follistatin in diabetic nephropathy(DN) through observing their gene expression in the kidney of diabetic rats.Methods:Male Wistar rats were randomized into normal control group(NC)and diabetes mellitus group(DM).Diabetes was induced by intraperitoneal injection of streptozotocin(STZ).Six rats were respectively sacrificed 4,8,12 and 16 weeks after model establishment in each group.The changes of kidney weight/body weight(KW/BW),urine albumin excretion rate(AER) and creatinine clearance rate(Ccr)were determined.Real time-PCR was applied to analyze the gene expression of activin A and follistatin in renal tissue.Results:Compared with NC group,KW/BW,AER and Ccr in DM group began to rise significantly(P0.01)from 8 weeks and reached peak value at 16 weeks.The PCR results demonstrated that significantly elevated activin A mRNA expression was observed in the DM group rats at 4 weeks and reached peak values at 12 weeks.By contrast,follistatin mRNA was abundant in the NC group rats.However,in the DM group rats,its expression began to decrease gradually from 4 weeks to 16 weeks.Conclusion:The imbalance of activin A and follistatin gene expression played an important role in the development of DN.
出处 《医学理论与实践》 2011年第12期1365-1367,共3页 The Journal of Medical Theory and Practice
基金 国家教育部高等学校博士学科点基金新教师基金资助(项目编号20090131120075)
关键词 糖尿病肾病 激活素A 卵泡抑素 Diabetic nephropathy Activin A Follistatin
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参考文献8

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同被引文献35

  • 1刘慧丽,袁立,杨云青.醛糖还原酶遗传缺失可显著减缓C57BL/6小鼠糖尿病肾病进程[J].中华糖尿病杂志,2010,2(5). 被引量:5
  • 2谈力欣,王战建.肥胖与糖尿病肾病的发病机制[J].中华糖尿病杂志,2010,2(5). 被引量:2
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  • 6Kumar PA, Brosius FC 3rd, Menon RK. The glomerular podocyte as a target of growth hormone action:implications for the pathogenesis of diabetic nephropathy. Curr Diabetes Rev, 2011, 7: 50-55.
  • 7Romero M, Ortega A, Izquierdo A, et al. Parathyroid hormone- related protein induces hypertrophy in podocytes via TGF-beta (1) and p27(Kipl): implications for diabetic nephropathy. Nephrol Dial Transplant, 2010, 25: 2447-2457.
  • 8Nagase R, Kajitani N, Shikata K, et al. Phenotypic change of macrophages in the progression of diabetic nephropathy; sialoadhesin- positive activated macrophages are increased in diabetic kidney. Clin Exp Nephrol, 2012, 16: 739-748.
  • 9Elmarakby AA, Abdelsayed R, Yao Liu J, et al. Inflammatory cytokines as predictive markers for early detection and progression of diabetic nephropathy. EPMA J, 2010, 1: 117-129.
  • 10Zhou T, He X, Cheng R, et al. Implication of dysregulation of the canonical wingless- type MMTV integration site (WNT) pathway in diabetic nephropathy. Diabetologia, 2012, 55: 255- 266.

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