Adiponectin inhibits cardiac arrest/cardiopulmonary resuscitationinduced apoptosis in brain by increasing autophagy involved in AdipoR1AMPK signaling.
Mol Med Rep
; 22(2): 870-878, 2020 08.
Article
em En
| MEDLINE
| ID: mdl-32468051
ABSTRACT
Emerging evidence suggests that both apoptosis and autophagy contribute to global cerebral ischemiareperfusion (GCIR)induced neuronal death, which results from cardiac arrest (CA). However, the mechanism of how GCIR may affect the balance between apoptosis and autophagy resulting from CA remains to be elucidated. Additionally, the role of adiponectin (APN) in reversing the apoptosis and autophagy induced by GCIR following cardiac arrestcardiopulmonary resuscitation (CACPR) is unclear. Thus, the aim of the present study was to investigate how GCIR affect the apoptosis and autophagy in response to CA and to clarify whether APN may alter the apoptosis and autophagy of neuronal death in GCIRinjured brain postCACPR. Using normal controls (Sham group) and two experimental groups [CACPRinduced GCIR injury (PCAS) group and exogenous treatment with adiponectin postCACPR (APN group)], it was demonstrated that both apoptosis and autophagy were observed simultaneously in the brain subjected to GCIR, but apoptosis appeared to be more apparent. Exogenous administration of APN significantly reduced the formation of malondialdehyde, a marker of oxidative stress and increased the expression of superoxide dismutase, an antioxidative enzyme, resulting in the stimulation of autophagy, inhibition of apoptosis and reduced brain tissue injury (P<0.05 vs. PCAS). APN treatment increased the expression of APN receptor 1 (AdipR1) and the phosphorylation of AMPactivated protein kinase (AMPK; Ser182) in brain tissues. In conclusion, GCIR induced apoptosis and inhibited autophagy, contributing to brain injury in CACPR. By contrast, APN reduced the brain injury by reversing the changes of neuronal autophagy and apoptosis induced by GCIR. The possible mechanism might owe to its effects on the activation of AMPK after combining with AdipR1 on neurons, which suggests a novel intervention against GCIR injury in CACPR conditions.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Autofagia
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Traumatismo por Reperfusão
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Transdução de Sinais
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Isquemia Encefálica
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Apoptose
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Adiponectina
Tipo de estudo:
Etiology_studies
Limite:
Animals
Idioma:
En
Revista:
Mol Med Rep
Ano de publicação:
2020
Tipo de documento:
Article