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J Biosci ; 43(2): 287-294, 2018 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-29872017

RESUMO

Non-alcoholic fatty liver disease (NAFLD) is one of the leading causes of chronic liver diseases around the world and commonly associated with insulin resistance and hyperlipidemia. Chlorogenic acid (CG) was reported to have insulinsensitizing activity and exert hypocholesterolemic and hypoglycemic effect. However, the involvement of CG in NAFLD remains far from being addressed. In this study, a high-fat diet-induced NAFLD rat model was used to investigate the biological roles and underlying mechanism of CG in NAFLD. The results showed that high-fat diet-fed rats exhibited an increase in body weight, glucose tolerance, liver injury, insulin resistance, as well as autophagy and C-Jun N-terminal kinase (JNK) pathway. Nevertheless, all these effects were alleviated by CG treatment. Moreover, angiotensin treatment in CG group activated the JNK pathway, and promoted autophagy, insulin resistance, and liver injury. In conclusion, our findings demonstrated that CG ameliorated liver injury and insulin resistance by suppressing autophagy via inactivation of JNK pathway in a rat model of NAFLD. Therefore, CG might be a potential application for the treatment of NAFLD.


Assuntos
Ácido Clorogênico/administração & dosagem , Resistência à Insulina/genética , Proteínas Quinases JNK Ativadas por Mitógeno/genética , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Animais , Autofagia/efeitos dos fármacos , Peso Corporal , Dieta Hiperlipídica , Modelos Animais de Doenças , Humanos , Hipoglicemiantes/administração & dosagem , Proteínas Quinases JNK Ativadas por Mitógeno/antagonistas & inibidores , Fígado/efeitos dos fármacos , Fígado/metabolismo , Fígado/patologia , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Masculino , Hepatopatia Gordurosa não Alcoólica/genética , Hepatopatia Gordurosa não Alcoólica/patologia , Ratos , Transdução de Sinais/efeitos dos fármacos
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