中文摘要：

目的: 糖尿病的 nephropathy 是糖尿病的主要复杂并发症和结束阶段的主要原因之一肾的疾病。在我们调查了的这研究，导致的胰岛素缺乏(标志) 在肾的 mesangial 房间(MC ) 并且在导致 STZ 的糖尿病的 rats.Methods 的肾变化: 有教养的老鼠肾的 MC 在标志媒介被孵化。房间增长用 BrdU 加入试金被分析。胰岛素受体(红外) 的表示，像胰岛素的生长 factor-1 受体(IGF-1R ) ， phosphorylated IGF-1R， fibronectin，和骨胶原 IV 与西方的污点分析被决定。导致 STZ 的糖尿病的老鼠与 IGF-1R 对手 picropodophyllin 被对待(PPP， 20 mg·； kg ⁻¹·d⁻¹, po ) 为 8 个星期。在老鼠是 euthanized 以后，血浆和肾是镇定的。在肾的外皮的 IGF-1 层次与 RT-PCR 或 ELISA 被测量。在肾的词法变化也是 examined.Results : 在标志媒介的孵化显著地增加了房间增长， fibronectin 的合成和骨胶原 IV，和在肾的 MC 的 IGF-1 和 IGF-1R 和 phosphorylated IGF-1R 的表示。有 PPP (50 nmol/L ) 的房间的预告的处理在房间增长和 fibronectin 和骨胶原 IV 的合成堵住了导致标志的增加；IGF-1R 击倒作为 PPP 显示出类似的效果。相反，有 IGF-1 (50 ng/mL ) 的房间的处理在房间增长加重了导致标志的增加。在糖尿病的老鼠， IGF-1 的表示， IGF-1R 和 phosphorylated 的肾， IGF-1R 显著地被提高。有 PPP 的糖尿病的老鼠的处理降低血葡萄糖层次，但是显著地压制了 TGF-β 的表示；，在肾的 fibronectin 和骨胶原 IV ，尿氮和 creatinine 的血浆层次，并且尿蛋白质 excretion.Conclusion :胰岛素缺乏在肾的 MC 和糖尿病的老鼠的肾增加 IGF-1 和 IGF-1R 的表达式，它贡献糖尿病的 nephropathy 的开发。

英文摘要：

Aim： Diabetic nephropathy is one of the major complications of diabetes and the major cause of end-stage renal disease. In this study we investigated the insulin deficiency （ID） induced changes in renal mesangial cells （MCs） and in the kidney of STZ-induced diabetic rats. Methods： Cultured rat renal MCs were incubated in ID media. Cell proliferation was analyzed using BrdU incorporation assay. The expression of insulin receptor （IR）, insulin-like growth factor-1 receptor （IGF-1R）, phosphorylated IGF-1R, fibronectin, and collagen IV was determined with Western blot analysis. STZ-induced diabetic rats were treated with an IGF-1R antagonist picropodophyllin （PPP, 20 mg.k-1.d-1, pc） for 8 weeks. After the rats were euthanized, plasma and kidneys were collected. IGF-1 levels in renal cortex were measured with RT-PCR or ELISA. The morphological changes in the kidneys were also examined. Results： Incubation in ID media significantly increased cell proliferation, the synthesis of fibronectin and collagen IV, and the expression of IGF-1 and IGF-1R and phosphorylated IGF-1R in renal MCs. Pretreatment of the cells with PPP （50 nmol/L） blocked ID-induced increases in cell proliferation and the synthesis of fibronectin and collagen IV; knockdown of IGF-1R showed a similar effect as PPP did. In contrast, treatment of the cells with IGF-1 （50 ng/mL） exacerbated ID-induced increases in cell proliferation. In the kidneys of diabetic rats, the expression of IGF-1, IGF-1R and phosphorylated IGF-1R were significantly elevated. Treatment of diabetic rats with PPP did not lower the blood glucose levels, but significantly suppressed the expression of TGF-β, fibronectin and collagen IV in the kidneys, the plasma levels of urinary nitrogen and creatinine, and the urinary protein excretion. Conclusion： Insulin deficiency increases the expression of IGF-1 and IGF-1R in renal MCs and the kidney of diabetic rats, which contributes to the development of diabetic nephropathy.