NLRC5 protects neurons from oxygen-glucose deprivation-induced injury through activating the Nrf2/HO-1 pathway.
J Recept Signal Transduct Res
; 41(1): 53-58, 2021 Feb.
Article
em En
| MEDLINE
| ID: mdl-32605461
ABSTRACT
NLRC5 is a member of the Nod-like receptor (NLR) family that has been found to be associated with the hepatic ischemia/reperfusion (I/R) injury. However, the role of NLRC5 in cerebral I/R has not been fully understood. The aim of the current study was to evaluate the effects of NLRC5 on primary hippocampal neuronal cells exposed to oxygen-glucose deprivation/reperfusion (OGD/R). Our results showed that the mRNA and protein levels of NLRC5 were significantly decreased in OGD/R-induced neurons. Overexpression of NLRC5 caused significant increase in cell viability, as well as decrease in ROS level. The bax expression was significantly decreased, while bcl-2 expression was increased in NLRC5-overexpressing neurons. Furthermore, increased nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression levels were observed in neurons transfected with pcDNA3.0-NLRC5. The mRNA levels of HO-1, NAD(P)Hquinone oxidoreductase 1 (NQO-1) and glutathione peroxidase 3 (GPx-3) were induced by NLRC5 overexpression in OGD/R-induced hippocampal neurons. Additionally, inhibition of Nrf2/HO-1 pathway abolished the protective effect of NLRC5 on cerebral I/R injury. In conclusion, these results indicated that NLRC5 protected hippocampal neurons from OGD/R-induced injury. The protective effects of NLRC5 were mediated by the Nrf2/HO-1 pathway. Thus, NLRC5 might serve as an effective target for the treatment of cerebral I/R injury.
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MEDLINE
Assunto principal:
Traumatismo por Reperfusão
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Fator 2 Relacionado a NF-E2
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Proteínas NLR
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Heme Oxigenase (Desciclizante)
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Neurônios
Idioma:
En
Ano de publicação:
2021
Tipo de documento:
Article