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参芪解毒汤对腺嘌呤所致慢性肾衰大鼠肾组织转化生长因子β1和Smad2、3表达的影响
引用本文:李婷婷,司国民,陈凤翠.参芪解毒汤对腺嘌呤所致慢性肾衰大鼠肾组织转化生长因子β1和Smad2、3表达的影响[J].中西医结合学报,2010,8(3):263-268.
作者姓名:李婷婷  司国民  陈凤翠
作者单位:1. 山东大学附属省立医院中医科,山东,济南,250021
2. 山东省乳山市中医院儿科,山东,乳山,264500
摘    要:目的:观察参芪解毒汤对腺嘌呤诱导的慢性肾衰大鼠肾脏组织转化生长因子p1(transforming growth factor—β1,TGF—β1)、Smad2和Smad3蛋白表达的影响,探讨参芪解毒汤治疗慢性肾衰竭(chronic renal failure,CRF)的作用机制。方法:将90只健康Wistar雄性大鼠随机分成正常对照组、模型组、氯沙坦组、低剂量参芪解毒汤组、中剂量参芪解毒汤组和高剂量参芪解毒汤组。腺嘌呤灌胃复制慢性肾衰大鼠模型,检测造模后血浆肌酐(ereatinine,Cr)、尿素氮(blood urea nitrogen,BUN)水平判断造模是否成功。治疗8周后,检测血浆Cr、BUN、三酰甘油(triacylglycerol,TAG)、胆固醇(cholesterol,Ch01)和白蛋白(albuminous,ALB)水平,HE染色观察大鼠肾脏组织病理学变化,蛋白印迹法检测肾组织TGF—β1、Smad2和Smad3蛋白的表达情况。结果:与治疗前相比,氯沙坦组和低、中、高剂量参芪解毒汤组Cr、BUN水平明显降低(Pd0.01);治疗后,各治疗组Cr、BUN和Chol水平低于模型组(P〈0.01,P〈0.05),ALB水平高于模型组(P〈0.01)。病理结果显示,各治疗组大鼠的肾组织病理损伤明显轻于模型组。蛋白印迹法检测提示各治疗组肾组织TGF—β1、Smad2和Smad3的蛋白表达低于模型组(P〈0.01)。结论:参芪解毒汤通过抑制TGF-β1/Smads信号传导通路发挥抗肾脏纤维化作用,减缓CRF进程。

关 键 词:慢性肾功能衰竭  复方  转化生长因子β1  Smad2  Smad3  大鼠

Effects of Shenqi Jiedu Decoction on expressions of transforming growth factor-β1, smad2 and smad3 in renal tissues of rats with chronic renal failure induced by adenine
Ting-ting LI,Guo-min SI,Feng-cui CHEN.Effects of Shenqi Jiedu Decoction on expressions of transforming growth factor-β1, smad2 and smad3 in renal tissues of rats with chronic renal failure induced by adenine[J].Journal of Chinese Integrative Medicine,2010,8(3):263-268.
Authors:Ting-ting LI  Guo-min SI  Feng-cui CHEN
Institution:1. Department of Traditional Chinese Medicine, Shandong Provincial Hospital, Shandong University, Jinan 250021, Shandong Province, China; 2. Department of Pediatrics, Rushan Hospital of Traditional Chinese Medicine, Rushan 264500, Shandong Province, China)
Abstract:Objective: To investigate the effects of Shenqi Jiedu Decoction (SQJDD), a compound traditional Chinese herbal medicine, on expressions of transforming growth factor beta1 (TGF-β1), smad2 and smad3 proteins in renal tissues of rats with chronic renal failure (CRF) induced by adenine, and to explore the mechanisms of SQJDD in treating CRF. Methods. Ninety healthy Wistar male rats were randomly divided into six groups: normal group, untreated group, Iosartan group, low-dose SQJDD group, medium-dose SQJDD group, and high-close SQJDD group.Rat model of CRF was established by feeding 2.5% adenine. Levels of plasma creatinine (Cr) and blood urea nitrogen (BUN) in different groups after model establishment were detected to estimate the renal function of rats with CRF. After eight-week treatment, levels of Cr, BUN, triacylglycerol (TAG), cholesterol (Chol) and albumin (ALB) in plasma were detected. Pathological changes of renal tissues were observed by HE staining. Protein expressions of TGF-β1, Smad2 and Smad3 in renal tissues were detected by Western blotting. Results: Compared with pretreatment, levels of Cr and BUN in the Iosartan group and the SQJDD groups were markedly decreased (P〈0. 01). After treatment, levels of Cr, BUN and Chol in all treated groups were lower than those in the untreated group (P〈0.01, P〈0. 05). Levels of ALB in all treated groups were higher than that in the untreated group (P〈0. 0]). Pathological lesions of renal tissues in all treated groups were lessened as compared with the untreated group (P〈0. 01). The Western blotting results showed that the protein expressions of TGF-β1, Smad2 and Smad3 in renal tissues in all treated groups were lower than those in the untreated group (P〈0.01). Conclusion: SQJDD can delay the progress of CRF by inhibiting TGF-131/Smads signal transduction pathway,
Keywords:Smad2  Smad3
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