Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Adicionar filtros








Intervalo de ano
1.
Chinese Journal of Applied Physiology ; (6): 314-317, 2014.
Artigo em Chinês | WPRIM | ID: wpr-236318

RESUMO

<p><b>OBJECTIVE</b>To investigate the influence of total flavonoids of epimedium (TFE) on the streptozocin (STZ)-induced kidney injury in diabetic rats and discuss the possible mechanism.</p><p><b>METHODS</b>Diabetes was produced by a single injection of streptozocin (40 mg/kg, iv) in male SD rats. The rats were randomly divided into three groups (n = 10): control group, model group and TFE group (100 mg/kg, ig). Animals were sacrificed 12 weeks later. The level of blood glucose, blood urea nitrogen (BUN) and creatinine (Cr) as well as the renal index were determined. Detect the specific biochemical of renal tissue: superoxide dismutase (SOD), malondialdehyde (MDA). Use masson staining to observe the morphology of the renal tissue. Immunohistochemistry was employed to determine the protein levels of transforming growth factor-beta1 (TGF-beta1).</p><p><b>RESULTS</b>Compared to control group, the enhancement of blood glucose, renal index, BUN and Cr was found in model group, which was significantly attenuated by treatment with TFE. Meanwhile, elevated MDA level in renal tissue as well as decreased SOD activities in renal tissue were significantly remitted by TFE. Furthermore, TFE decreased the expression of TGF-beta1.</p><p><b>CONCLUSION</b>TFE can evidently relieve renal damage in rats with diabetic nephropathy induced by STZ, which might be related to antioxidation and modulating the expression of TGF-beta1 protein.</p>


Assuntos
Animais , Masculino , Ratos , Diabetes Mellitus Experimental , Metabolismo , Nefropatias Diabéticas , Metabolismo , Epimedium , Química , Flavonoides , Farmacologia , Rim , Metabolismo , Ratos Sprague-Dawley
2.
Chinese Journal of Applied Physiology ; (6): 445-448, 2014.
Artigo em Chinês | WPRIM | ID: wpr-243464

RESUMO

<p><b>OBJECTIVE</b>To investigate the effect of ursolic acid (UA) on the alloxan-induced kidney injury in diabetic mice and explored its possible mechanisms.</p><p><b>METHODS</b>Diabetes mellitus was induced in male Kunming mice by an injection of alloxan (70 mg/kg, i.v.). After 72 hours, blood glucose levels were detected and mice with blood glucose levels over 13.9 mmol/L were considered as diabetic and selected for further experiment. Thirty mice were randomly divided into three groups: control, diabetic and diabetic + UA(35 mg/kg/d, i.g. continuously for 8 weeks). Blood glucose concentration, organ coefficient of kidney, blood urea nitrogen (BUN), creatinine (Cr) as well as renal tissue levels of superoxide dismutase (SOD), methane dicarboxylic aldehyde (MDA), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were determined. Pathology of the renal tissue was measured by hematoxylin-eosin staining.</p><p><b>RESULTS</b>Compared to the control group, blood glucose, organ coefficient of kidney, BUN and Cr increased significantly. In addition, SOD activities was reduced markedly and levels of MDA and inflammatory factors (TNF-α, IL-6) increased significantly. Renal cells from model group rats showed atrophy and disordered after HE staining and infiltration of inflammatory cells also appeared in renal tissue of the model group. These changes were significantly attenuated in the diabetic group treated with UA.</p><p><b>CONCLUSION</b>UA can significantly relieve renal damage in mice with diabetic nephropathy induced by alloxan, which might be related to decreased blood glucose level, antioxidation effect and inhibiting the production of inflammatory factors such as TNF-α and IL-6.</p>


Assuntos
Animais , Masculino , Camundongos , Aloxano , Antioxidantes , Metabolismo , Glicemia , Nitrogênio da Ureia Sanguínea , Creatinina , Metabolismo , Diabetes Mellitus Experimental , Nefropatias Diabéticas , Tratamento Farmacológico , Interleucina-6 , Metabolismo , Rim , Superóxido Dismutase , Metabolismo , Triterpenos , Farmacologia , Fator de Necrose Tumoral alfa , Metabolismo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA