Abstract

Objectivec-myc has been reported to attenuate ischemia stroke (IS). We initiated the research to uncover the molecular mechanism of c-myc with regard to microRNA (miR)-200b-5p/Sirtuin1 (SIRT1) axis. MethodsAn IS mouse model was prepared by middle cerebral artery occlusion (MCAO). Measurements of c-myc, miR-200b-5p and SIRT1 levels in MCAO mice were conducted. c-myc, miR-200b-5p and SIRT1 expression levels in MCAO mice were detected. The neurological function, production of inflammatory cytokines, neuronal apoptosis, brain tissue pathology and neuronal survival of MCAO mice were observed. Resultsc-myc and SIRT1 levels went downward while miR-200b-5p expression went upward in MCAO mice. Elevation of c-myc or suppression of miR-200b-5p improved neurological function, reduced inflammation and neuronal apoptosis, and attenuated brain tissue pathology and neuronal survival of MCAO mice. Enhancement of miR-200b-5p or knockdown of SIRT1 weakened c-myc-induced protection against MCAO-induced brain injury in mice. ConclusionOverall, c-myc protects mice from IS through elevating miR-200b-5p-targeted SIRT1 expression.

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