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山莨菪碱对梗阻性肾病大鼠肾间质纤维化的抑制
引用本文:唐云海,朱春玲. 山莨菪碱对梗阻性肾病大鼠肾间质纤维化的抑制[J]. 贵阳医学院学报, 2010, 35(1): 26-29
作者姓名:唐云海  朱春玲
作者单位:贵阳医学院附院,肾内科,贵州,贵阳,550004
摘    要:目的:探讨山莨菪碱对梗阻性肾病大鼠肾间质纤维化(RIF)的影响及机制。方法:将27只SD大鼠随机分为假手术组(SHAM,S组)、模型组(UUO,U组)及山莨菪碱治疗组(A组,14mg·kg^-1·d^-1)。U组和A组采用单侧输尿管结扎术(UUO)制作肾小管间质纤维化的动物模型。术后第11天处死大鼠,肾组织HE染色及Masson染色后进行图像分析,评定各组肾小管间质损害及肾间质纤维化状况;用免疫组织化学方法检测各组大鼠肾间质的转化生长因子-β1(TGF—β1)的表达。结果:U组肾小管间质损伤指数(TDI)及肾间质纤维化指数(TFI)均明显高于S组(P〈0.01);U组TGF—β1的表达均明显高于S组(P〈0.01);A组的上述各指标分别较U组降低(P〈0.05);TDI、TFI分别与TGF—β1的表达呈正相关。结论:山莨菪碱对梗阻性肾病大鼠肾间质纤维化具有一定的抑制作用,其机制可能是抑制肾间质细胞TGF—β1的表达而在一定程度上减轻了RIF。

关 键 词:山莨菪碱  纤维化    转化生长因子β  大鼠,Sprague—Dawley  肾间质纤维化

An Experimental Study on the Inhibitory Effect of Anisodamine to Renal Tubulointerstitial Fibrosis in Obstructive Nephropathy Rats
TANG Yunhai,ZHU Chunling. An Experimental Study on the Inhibitory Effect of Anisodamine to Renal Tubulointerstitial Fibrosis in Obstructive Nephropathy Rats[J]. Journal of Guiyang Medical College, 2010, 35(1): 26-29
Authors:TANG Yunhai  ZHU Chunling
Affiliation:(Department of Nephrology and Rheumatism, The Affiliated Hospital of Guiyang Medical College, Guiyang 550004, Guizhou, China)
Abstract:Objective: To observe the influence of anisodamine to renal tubulointerstitial fibrosis of obstructive nephropathy rats and its possible mechanism. Methods: Renal interstitial fibrosis (RIF) models were established by Unilateral Ureteral Obstruction (UUO) method. Twenty-seven male Sprague-Dawley rats were randomly divided into 3 groups: sham-operated group (group S), UUO group (group U) and anisodamine (14 mg · kg^-1· d^-1) treated group (group A). All of the rats were killed on the 11^st day of the experiment. Sections of renal tissue were stained with HE or Masson methods, and image analysis was carried out to evaluate the damage in renal tubulointerstitium and the fibrosis of renal interstitium. The expression of transforming growth faetor-β1 ( TGF-β1 ) was determined with immunohistochemistry method. Results: Tubulointerstitial damage index (TDI) , tubulointerstitial fibrosis index (TFI) , and expression of TGF-β1 in group U were significantly higher than those in group S (P 〈0.01). These indexes were obviously lower in group A than those in group U (P 〈0. 05). TDI and TFI positively correlated with expression of TGF-β1 respectively. Conclusions: Anisodamine has inhibitory effect to RIF, and the possible mechanism might be that anisodamine inhibits the expression of-TGF-β1, which leads to the relief of renal tubulointerstitial fibrosis to some extent.
Keywords:anisodamine  fibrosis  kidney  transforming growth factor beta  rats, Sprague-dawley  renal tubulointerstitial fibrosis
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