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

Base de dados
Ano de publicação
Tipo de documento
Intervalo de ano de publicação
1.
J Diabetes Investig ; 14(1): 28-36, 2023 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-36345578

RESUMO

AIMS/INTRODUCTION: Emerging evidence has suggested the detrimental role of oxidative stress in aggravating ischemia and reperfusion (IR) injury in diabetic livers. Interplay between oxidative stress and mitophagy has been shown. However, the role and mechanism of mitophagy in regulating oxidative stress and IR injury in diabetic livers remain unclear. MATERIALS AND METHODS: Wild-type and db/db (DB) mice were subjected to a partial warm liver IR model. Liver injury, oxidative stress, mitophagy and related molecular pathways were analyzed. RESULTS: Here, we found that increased liver IR injury was observed in DB mice, as evidenced by higher levels of serum alanine aminotransferase and serum aspartate, worsened liver architecture damage and more hepatocellular death. DB mice also showed increased mitochondrial oxidative stress. Mitochondrial reactive oxygen species scavenge alleviated liver IR injury in DB mice. Mechanistic analysis showed that 5' adenosine monophosphate-activated protein kinase-mediated mitophagy was suppressed in DB mice post-IR. Pharmacological activation of 5' adenosine monophosphate-activated protein kinase by its agonist effectively restored mitophagy activation, leading to decreased mitochondrial oxidative stress and attenuated liver IR injury in DB mice. CONCLUSIONS: Our findings showed that diabetes increased oxidative stress to exacerbate liver IR injury by impairing 5' adenosine monophosphate-activated protein kinase-mediated mitophagy. Strategies targeting oxidative stress and mitophagy might provide a promising approach to ameliorate liver IR injury in diabetes patients.


Assuntos
Diabetes Mellitus Experimental , Hepatopatias , Traumatismo por Reperfusão , Camundongos , Animais , Mitofagia , Diabetes Mellitus Experimental/complicações , Diabetes Mellitus Experimental/metabolismo , Traumatismo por Reperfusão/complicações , Traumatismo por Reperfusão/metabolismo , Fígado/metabolismo , Estresse Oxidativo , Hepatopatias/etiologia , Isquemia/metabolismo , Proteínas Quinases Ativadas por AMP/metabolismo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA