MicroR-146 protects against rat ischemia-reperfusion injury by targeting NF-κB-mediated PI3K/AKT/mTOR signaling pathway
Abstract MicroR-146 (miR-146) plays crucial roles in attenuating nerve injury during cerebral ischemia-reperfusion (I/R) injury. The purpose of this study was to investigate the neuroprotective effect of miR-146 against cerebral I/R injury. Rat model of cerebral I/R injury was established using 4-ve...
| Autores: | , , , , , , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2022 |
| País: | Brasil |
| Institución: | Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA) |
| Repositorio: | Food Science and Technology (Campinas) |
| Idioma: | inglés |
| OAI Identifier: | oai:scielo:S0101-20612022000100401 |
| Acceso en línea: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100401 |
| Access Level: | acceso abierto |
| Palabra clave: | miR-146 cerebral I/R injury apoptosis PI3K/AKT/mTOR |
| Sumario: | Abstract MicroR-146 (miR-146) plays crucial roles in attenuating nerve injury during cerebral ischemia-reperfusion (I/R) injury. The purpose of this study was to investigate the neuroprotective effect of miR-146 against cerebral I/R injury. Rat model of cerebral I/R injury was established using 4-vessel occlusion and reperfusion. In this study, miR-146 expression was significantly decreased in neurons in cerebral I/R injury rat compared to sham group. In addition, miR-146+/+ significantly decreased inflammatory cytokines, oxidative stress, neuron cell apoptosis and the infarct size in cerebral I/R injury rats (p<0.05). Transfection of miR-146 reduced apoptosis, autophagy and autophagy-related proteins LC-3, Beclin-1 and increased p62 in the neuron cells compared to control group. Furthermore, overexpression of miR-146 was indicated to directly targeting NF-κB and activating PI3K/AKT/mTOR expression in neuron cells. In conclusion, these findings suggested that miR-146 could protect against rat ischemia-reperfusion injury by targeting NF-κB-mediated PI3K/AKT/mTOR signaling pathway, which offered a potential molecular for the treatment of cerebral I/R injury. |
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