MicroRNA-454 modulates the oxidative stress and neuronal apoptosis after cerebral ischemia/reperfusion injury via targeting NADPH oxidase 4 (NOX4).
J Biochem Mol Toxicol
; 36(10): e23153, 2022 Oct.
Article
em En
| MEDLINE
| ID: mdl-36043333
ABSTRACT
To investigate the function of miR-454 in ischemic stroke, this study was carried out. Cerebral ischemia/reperfusion (I/R) injury animal model and a SHSY5Y cell culture model of oxygen-glucose deprivation/reoxygenation (OGD/R) were constructed. The effects of miR-454 were detected by evaluating the levels of biochemical markers, gene expression, and pathophysiological markers. The results showed that NOX4 level was elevated, while miR-454 expression was reduced in I/R brain samples and in OGD/R-treated cells. The miR-454 agomir declined NOX4 level and reactive oxygen species (ROS) production in rats suffering from I/R. Furthermore, microRNA-145 (miR-454) overexpression inhibited NOX4 level and ROS production in cells treated by OGD/R and decreased luciferase activity in cells transfected with NOX4-wild type (WT) reporter plasmid. Meanwhile, our results proved that the protected effects of miR-454 on SH-SY5Y cells treated by OGD/R were reversed by pcDNA-NOX4 transfection. MiR-454 protected animals from brain injury induced by cerebral I/R via directly regulating its target gene NOX4, illustrating a curatively potential target for treating ischemic stroke.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Traumatismo por Reperfusão
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Isquemia Encefálica
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MicroRNAs
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AVC Isquêmico
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Neuroblastoma
Limite:
Animals
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Humans
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article