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1.
China Journal of Chinese Materia Medica ; (24): 938-945, 2015.
Artigo em Chinês | WPRIM | ID: wpr-330206

RESUMO

<p><b>OBJECTIVE</b>To investigate the effect of compound Coptidis Rhizoma capsule (CCRC) on unbalanced expression of renal tissue TGF-β1/BMP-7 and Smad signaling pathway in rats with early diabetic nephropathy (DN), and discuss CCRC's effect on DN rats with early diabetic nephropathy and its possible mechanism.</p><p><b>METHOD</b>DN model rats were established by injecting streptozotocin (STZ). The rats were randomly divided into seven groups: the normal group, the model group, the enalapril treatment group, the xiaoke pill treatment group and three CRCC treatment groups. They were orally administered once a day for five weeks. The fasting blood glucose (FBG), blood urea nitrogen (BUN), serum creatinine (Scr), insulin (Ins), 24 h urinary protein (24 h Upro) and 24 h urinary microalbumin (24 h UmAlb) were tested. The pathological changes in renal tissues were examined by optical microscopy. Immuno- histochemical measures were used to detect the expressions of TGF-β1, BMP-7, Smad2/3, Smad1/5, and Smad7 protein, and RT-PCR was used to detect TGF-β1 mRNA and BMP-7 mRNA in renal tissues.</p><p><b>RESULT</b>Compared with model group, BUN, Scr, Ins, 24 h Upro and 24 h UmAlb levels decreased at different degrees in CCRC treatment groups; the abnormal pathomorphology in renal tissue was improved; immunohistochemistry results showed that the expression of TGF-β1 and Smad2/3 were reduced, while the expression of BMP-7, Smad1/5 and Smad7 increased in CRCC treatment groups; the expression of TGF-β1 mRNA were reduced, but the expression of BMP-7 mRNA had no obvious change in CRCC treatment groups.</p><p><b>CONCLUSION</b>CRCC can improve the early renal function, delay the progression of chronic renal pathology and maintain the dynamic balance of TGF-β1/BMP-7 expression in renal tissues of DN rats. The mechanism may be related to down-regulation of renal TGF-β1 and up-regulation of BMP-7 through Smad signaling pathway.</p>


Assuntos
Animais , Humanos , Masculino , Ratos , Proteína Morfogenética Óssea 7 , Genética , Metabolismo , Coptis , Química , Nefropatias Diabéticas , Tratamento Farmacológico , Genética , Metabolismo , Regulação da Expressão Gênica , Rim , Metabolismo , Ratos Sprague-Dawley , Rizoma , Química , Transdução de Sinais , Proteínas Smad , Genética , Metabolismo , Fator de Crescimento Transformador beta1 , Metabolismo
2.
China Journal of Chinese Materia Medica ; (24): 3604-3610, 2012.
Artigo em Chinês | WPRIM | ID: wpr-346898

RESUMO

<p><b>OBJECTIVE</b>To investigate the effect of berberine (BBR) on unbalanced expression of renal tissue TGF-beta1/SnoN and Smad signal pathway in rats with early diabetic nephropathy (DN), and discuss BBR's effect on DN rats with early diabetic nephropathy and its possible mechanism.</p><p><b>METHOD</b>DN rat model were established by injecting streptozotocin (STZ). The rats were divided into six groups: the control group, the model group, three BBR (50, 100, 200 mg x kg(-1)) treatment groups and the enalapril treatment group. They were orally administered once a day for five weeks. The fasting blood glucose (FBG), blood urea nitrogen (BUN), serum creatinine (Scr), urinary protein (24 h Upro) and urinary microalbumin (24 h UmAlb) were tested. The pathological changes in renal tissues were examined by optical microscopy. Immunohistochemical measures were used to detect the expressions of TGF-beta1, SnoN, Smad2/3 and Smad7 protein, and RT-PCR was used to detect TGF-beta1 mRNA in renal tissues.</p><p><b>RESULT</b>Compared with the model group, BBR-treated groups showed significant decrease in FBG, BUN, Scr, 24 h Upro, 24 h UmAlb, TGF-beta1 protein, mRNA and Smad2/3 protein, abnormal morphological improvement in renal tissues, and notable increase in the expressions of SnoN and Smad7 protein.</p><p><b>CONCLUSION</b>BBR can maintain the dynamic balance in TGF-beta1/SnoN expression in renal tissues through Smad signaling pathway, so as to mitigate renal functional disorder in DN rats and delay DN and its development.</p>


Assuntos
Animais , Humanos , Masculino , Ratos , Berberina , Nefropatias Diabéticas , Tratamento Farmacológico , Genética , Metabolismo , Expressão Gênica , Rim , Metabolismo , Proteínas do Tecido Nervoso , Genética , Metabolismo , Ratos Sprague-Dawley , Transdução de Sinais , Proteínas Smad , Genética , Metabolismo , Fatores de Transcrição , Genética , Metabolismo , Fator de Crescimento Transformador beta1 , Genética , Metabolismo
3.
China Journal of Chinese Materia Medica ; (24): 68-72, 2008.
Artigo em Chinês | WPRIM | ID: wpr-324296

RESUMO

<p><b>OBJECTIVE</b>To explore the effect and mechanism of compound Rhizoma Coptidis capsule (CRCC) on diabetic nephropathy in experimental rats.</p><p><b>METHOD</b>The rat model of early diabetic nephropathy was induced by injection of streptozotocin (STZ). The rats were divided into 6 groups: normal control group, model group, 3 CRCC treatment groups and XKW treatment group. The fasting blood glucose (FBG), blood urea nitrogen (BUN), creatinine (Cr), insulin (Ins) and urinary protein (Upro) were tested 30 days later. The expression of transforming growth factor-beta1 (TGF-beta1) and type IV collagen (IV-C) proteins and the pathological changes in renal tissue of diabetic rats with nephropathy were observed by optical micrography.</p><p><b>RESULT</b>CRCC could reduce the levels of FBG, BUN, Cr, Upro and the expression of TGF-beta1 and IV-C proteins, and alleviate pathological lesion in renal tissue of diabetic rats with nephropathy.</p><p><b>CONCLUSION</b>CRCC may protect the renal function and slow down the progression of diabetic nephropathy in rats by suppressing the expression of TGF-beta1 and IV-C proteins in renal tissue.</p>


Assuntos
Animais , Masculino , Ratos , Colágeno Tipo IV , Metabolismo , Nefropatias Diabéticas , Metabolismo , Medicamentos de Ervas Chinesas , Farmacologia , Regulação da Expressão Gênica , Imuno-Histoquímica , Rim , Metabolismo , Patologia , Plantas Medicinais , Química , Ratos Wistar , Fator de Crescimento Transformador beta1 , Metabolismo
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