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Effects of fenofibrate and rosiglitazone on the signal passway of p38MAPK in glomerular mesangial cells cultivated in high concentration of glucose / 中国临床药理学与治疗学
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-565659
Biblioteca responsável: WPRO
ABSTRACT

AIM:

To investigate the effects of fenofibrate(FB) and rosiglitazone(RG) on the signal passway of p38 mitogen-activated protein kinases(p38 MAPK) in glomerular mesangial cells cultivated in high concentration of glucose.

METHODS:

Rat mesangial cells(MC) were incubated in 5.5 mmol/L normal control glucose,25 mmol/L high glucose(HG),HG+100 ?mol/L fenofibrate(FB+HG),HG+20 ?mol/L rosiglitazone maleate(RG+HG),respectively.The fibronectin(FN) and type Ⅳ collagen(Col-Ⅳ) in supernatant were determined by ELISA.The expressions of p38MAPK and phospho-p38MAPK proteins in cytoplasm and nuclei were detected by Phospho-ELISA.The mRNA expression of p38MAPK was detected by semi-quantitative reverse transcription polymerase chain reaction(RT-PCR).

RESULTS:

Compared with normal control,the Col-Ⅳand FN in supernatant in HG group were much higher,the expression of p-p38MAPK was increased in cytoplasms and nuclei.Col-Ⅳ and FN were obviously decreased with the treatment of FB or RG,and the expression of p-p38MAPK in nuclei was down-regulated,but the expression of p-p38MAPK in intracytoplasm had no changes.There were no significant differences of the expressions of total protein and mRNA of p38MAPK among four groups.

CONCLUSION:

FB,RG could inhibit the activation of p38MAPK in nuceli of MC cultivated in high concentration of glucose,and then reduce the synthesis of extracellular matrix.

Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Clinical Pharmacology and Therapeutics Ano de publicação: 2002 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Clinical Pharmacology and Therapeutics Ano de publicação: 2002 Tipo de documento: Artigo
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