摘要
目的 :观察慢性肾功能衰竭 ( CRF)转化生长因子β1 ( TGFβ1 )的表达 ,探讨中药肾衰 3号颗粒剂缓解 CRF恶化的作用机制。方法 :6 0只 Wistar大鼠随机分为正常组、模型组、中药低剂量组、中药高剂量组和洛丁新组。从大鼠尾静脉注射阿霉素 7.5 m g/kg造成阿霉素肾病模型 ;观察 2 4 h尿蛋白量、血肌酐 ( SCr)、尿素氮 ( BU N)、肌酐清除率 ( CCr)及肾小管间质病理变化 ;免疫组化法观察 TGFβ1 、血小板源性生长因子 β( PDGFβ)在肾脏的表达及药物影响。结果 :中药高剂量组尿蛋白含量、SCr、BUN改善程度均较其他治疗组明显 ,与模型组相比差异显著 ( P均 <0 .0 1) ;肾小管间质病变减轻最为明显 ;TGFβ1 主要表达于肾小球内皮细胞和肾小管上皮细胞 ,PDGFβ主要表达于肾小球系膜区及肾小管近曲和远曲上皮细胞 ,且阳性表达率均为各组最低 ( TGFβ1 为 2 5 .0 % ,PDGFβ为 33.3% )。结论 :肾衰 3号颗粒剂对 CRF的保护作用机制可能是通过下调 TGFβ1 表达而减少肾小球细胞外基质沉积 ,下调 PDGFβ表达而减少肾小球系膜细胞过度增殖。
Objective: To observe transforming growth factorβ 1(TGFβ 1) expression in chronic renal failure(CRF) rats, and investigate the effect of Shenshuai palletⅢ(SSPⅢ,肾衰3号颗粒剂) on slowing down the speed of deterioration of CRF.Methods: Sixty Wistar rats were randomly divided into five groups: normal group, model group, SSPⅢ low dosage group(SSPⅢL), SSPⅢ high dosage group(SSPⅢH), and lolensin group. The adriamycin (ADR)nephritis rats models were established by injecting ADR 7.5 mg/kg from tail vein. The changes of uria protein of 24 hours,levels of serum creatinine(SCr), blood urea nitrogen(BUN), creatinine clearence(CCr) and the pathologic changes of renal tubule interstitium were observed. The expression of TGFβ 1 and plateletderived growth factorβ(PDGFβ) in kidney, and the SSPⅢ on it were observed by immunhistochemistry.Results: The levels of uria protein of 24 hours, SCr and BUN were improved obviously in the SSPⅢH group compared to the other treatment group, and the differences were significant in the treatment groups compared to the model group (all P <0.01). In the SSPⅢH group, the pathologic change of renal tubule interstitium were mildest compared to the other treatment group; the TGFβ 1 mainly expressed in the glomerulus endothelial cell and renal tubule epithelial cell; the PDGFβ mainly expressed at glomerulus mesentery district,renal tubule proximal tubule and distal tubule epithelial cell. The positive rate of expression of TGFβ 1(25 0%) and PDGFβ(33 3%) were the lowest in SSPⅢH group.Conclusion: The protective mechanism of SSPⅢ on CRF maybe decrease the deposition of the glomerular extra cellular matrix perhaps by down regulating the expression of TGFβ 1, and decrease the excessive proliferation of the glomerulus mesentery cell perhaps by downregulating the expression of PDGFβ.
出处
《中国中西医结合急救杂志》
CAS
2004年第6期345-348,共4页
Chinese Journal of Integrated Traditional and Western Medicine in Intensive and Critical Care
基金
黑龙江省政府科研基金资助项目 (GC0 114 5 0 1)
