早期糖尿病大鼠肾组织尾加压素Ⅱ表达的实验研究(1)
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2010年3月25日
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[摘要] 目的:探讨早期糖尿病大鼠肾组织中尾加压素Ⅱ(urotensin Ⅱ,UⅡ)的表达及其意义。方法:用链脲佐菌素(STZ)诱导糖尿病大鼠模型,将实验动物分为正常对照组(C组)、糖尿病组(D组)和胰岛素干预组(Y组)。5周后收集肾组织,观察各组肾脏病理情况及UⅡ在肾组织中的表达。结果:处理5周后,与C、Y组比较,D组肾小球肥大、肾小球表面积显著增大,小管扩张,上皮细胞肿胀;D组肾小管上皮细胞UⅡ表达明显升高(与C组比较,P<0.05);Y组肾小管上皮细胞UⅡ表达有不同程度的下降(与D组比较,P<0.05)。结论:STZ诱导的早期糖尿病大鼠肾小管上皮细胞UⅡ表达明显上调;应用胰岛素严格控制血糖可部分下调肾组织UⅡ的表达。UⅡ在STZ诱导的早期糖尿病大鼠肾脏病变的发展过程中可能起一定作用。
[关键词] 尾加压素Ⅱ;糖尿病肾病;免疫组织化学;大鼠
[中图分类号] R-332 [文献标识码]A [文章编号]1674-4721(2010)03(c)-019-03
Experimental study on expression of urotensin Ⅱ in renal tissue in STZ-induced early rats with diabetes
LIU Changbo,HUANG Huaying,CHEN Hanwei,FENG Zhengping,ZHENG Linhong
(Zengcheng People′s Hospital,Zengcheng 511300, China)
[Abstract] Objective: To explore expression of urotensin Ⅱ in renal tissue in STZ-rats with diabetes and its significance.Methods: Diabetic rats were induced by streptozocin(STZ), the experimental rats were randomly divided into three groups:normal control group(group C), diabetic rats(group D) and diabetic rats treated by insulin(group Y). 5 weeks later, the kidney specimens in different group were randomly collected and fixed in formalin and embedded with paraffin. The expression level and distribution of urotensin Ⅱ were evaluated withimmunohistochemistry technique. Results: After treatment of 5 weeks, urotensin Ⅱ levels in renal tubule epithelial cells in group D increased remarkably compared with those in group C(P<0.05),while UⅡ levels renal glomerulus endothelial cells in group D didn′t increase markedly.In comparison with group D,urotensinⅡ levels were significantly reduced in group Y(P<0.05). Conclusion: The expression of UⅡ in renal tubule epithelial cells upregulated markedly in STZ-rats with diabetes;rigid controls of blood glucose by insulin can partly downregulate the expression of UⅡin renal tissue.UrotensinⅡmight play a role in the development of renal pathological changes in STZ-rats with diabetes.
[Key words] Urotensin Ⅱ; Diabetic nephropathy; Immunohistochemistry; Rats
研究证实人类尾加压素Ⅱ(urotensinⅡ,UⅡ)在糖尿病肾病患者肾小管内皮细胞及间质中出现大量异常表达,它在糖尿病肾病的发生发展中起了何种作用,目前尚不明确。为此,笔者采用STZ诱导的早期糖尿病大鼠模型观察糖尿病肾组织中UⅡ的表达及其意义 ......
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