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• W2564861511 abstract "Microglia mediated inflammation contributes to intracerebral hemorrhage (ICH) induced secondary injury. Activated microglia has dual functions as pro-inflammatory (M1) and anti-inflammatory (M2) factors in brain injury and repair. MiR-124 is a potent anti-inflammatory agent which affects microglia after brain injury. However, the potential of modulating the M1/M2 polarization of microglia after ICH has not been reported. In this experiment, we detected the effect of miR-124 on the M1/M2 polarization state. In addition, the ability miR-124 to subsequently impacted neurological deficit and cerebral water content of ICH mice were studied. Furthermore, the relationship between miR-124 and C/EBP-α target was detected. We found that miR-124 significantly increased in M2-polarized microglia. Transduction of miR-124 mimics decreased proinflammatory cytokine levels. A coculture model of microglia and neuron indicated that M2-polarized microglia protected neuron damage. Furthermore, miR-124 banded to the 3-untranslated region of C/EBP-α and downregulated its protein levels. In vivo, infusion of miR-124 decreased brain levels of C/EBP-α and significantly reduced brain injury in ICH mice. Thus, miR-124 ameliorated ICH-induced inflammatory injury by modulating microglia polarization toward the M2 phenotype via C/EBP-α. MiR-124 regulatory mechanisms also might represent new therapeutic strategy in ICH." @default.
• W2564861511 created "2017-01-06" @default.
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• W2564861511 date "2017-02-01" @default.
• W2564861511 modified "2023-09-25" @default.
• W2564861511 title "MiR-124 contributes to M2 polarization of microglia and confers brain inflammatory protection via the C/EBP-α pathway in intracerebral hemorrhage" @default.
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• W2564861511 doi "https://doi.org/10.1016/j.imlet.2016.12.003" @default.
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