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为了初步阐明尿毒清颗粒(uremic clearance granule,UCG)在体内调控转化生长因子(transforming growth factor,TGF)-β1/SnoN/Smads信号通路而改善肾间质纤维化(renal interstitial fibrosis,RIF)的作用和机制,将15只大鼠随机分为正常组、模型组、尿毒清组。采用腺嘌呤灌胃联合单侧输尿管结扎术(unilateral ureteral obstruction,UUO)建立肾衰竭模型。造模后,3组大鼠分别给予UCG悬浊液或蒸馏水,共3周,其间,检测大鼠体重、24 h尿蛋白排泄量(urinary protein excretion,Upro);给药3周后,处死全部大鼠,抽取血液,摘除双肾,称重,观察肾脏外观和肾组织形态特征,检测血清生化指标和肾组织TGF-β1,SnoN,磷酸化Smad2/3(phosphorylated Smad2/3,p-Smad2/3)以及Smad7蛋白表达量。结果表明,经UCG干预后,模型鼠一般情况,肾脏外观、血清肌酐(serum creatinine,Scr)、血清尿素氮(blood urea nitrogen,BUN)、尿酸(uric acid,UA)、白蛋白(albumin,Alb)、Upro以及肾组织形态均得到不同程度的改善;UCG还可以下调模型鼠肾组织TGF-β1,p-Smad2/3蛋白表达水平,上调SnoN,Smad7蛋白表达水平。总之,UCG可能在体内多靶点地调控TGF-β1/SnoN/Smad信号通路,从而,减少细胞外基质(extracellular matrix,ECM)合成,延缓肾衰竭进展。
To clarify the effect of uremic clearance granule (UCG) on renal interstitial fibrosis (RIF), which regulates the transforming growth factor (TGF) -β1 / SnoN / Smads signaling pathway in vivo And mechanism, 15 rats were randomly divided into normal group, model group, nootropic group. Renal failure model was established by adenine gavage combined with unilateral ureteral obstruction (UUO). After modeling, the rats in each group were given UCG suspension or distilled water for 3 weeks, respectively, during which they were tested for body weight and urinary protein excretion (Upro); 3 weeks after the administration, all Rats were sacrificed and the kidneys were removed. The kidneys were removed and the kidneys were removed. The kidney appearance and morphological features were observed. Serum biochemical parameters and expressions of TGF-β1, SnoN, phosphorylated Smad2 / 3, 3) and Smad7 protein expression. The results showed that after the intervention of UCG, the general situation of the model rats, the appearance of the kidney, serum creatinine (Scr), serum urea nitrogen (BUN), uric acid (UA), albumin ), Upro and renal tissue morphology were improved to varying degrees; UCG can also downregulate the expression of TGF-β1, p-Smad2 / 3 in renal tissue and up-regulate the expression of SnoN and Smad7 in model mice. In conclusion, UCG may regulate the TGF-β1 / SnoN / Smad signaling pathway in vivo in a multi-target manner, thereby reducing the synthesis of extracellular matrix (ECM) and slowing the progression of renal failure.