Long non-coding RNA MEG3 regulates autophagy after cerebral ischemia/reperfusion injury

Long non-coding RNA MEG3 regulates autophagy after cerebral ischemia/reperfusion injury

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Severe cerebral ischemia/reperfusion injury has been shown to induce high-level autophagy and neuronal death.Therefore, it is extremely important to search chocolate chip cookie purse for a target that inhibits autophagy activation.Long non-coding RNA MEG3 participates in autophagy.However, it remains unclear whether it can be targeted to regulate cerebral ischemia/reperfusion injury.

Our results revealed that in oxygen and glucose deprivation/reoxygenation-treated HT22 cells, MEG3 expression was obviously upregulated, and autophagy was increased, while knockdown of MEG3 expression greatly reduced autophagy.Furthermore, MEG3 bound miR-181c-5p and inhibited its expression, while miR-181c-5p bound to autophagy-related gene ATG7 and inhibited its expression.Further experiments revealed that mir-181c-5p overexpression reversed bilstein shocks jeep xj the effect of MEG3 on autophagy and ATG7 expression in HT22 cells subjected to oxygen and glucose deprivation/reoxygenation.In vivo experiments revealed that MEG3 knockdown suppressed autophagy, infarct volume and behavioral deficits in cerebral ischemia/reperfusion mice.

These findings suggest that MEG3 knockdown inhibited autophagy and alleviated cerebral ischemia/reperfusion injury through the miR-181c-5p/ATG7 signaling pathway.Therefore, MEG3 can be considered as an intervention target for the treatment of cerebral ischemia/reperfusion injury.This study was approved by the Animal Ethics Committee of the First Affiliated Hospital of Zhengzhou University, China (approval No.XF20190538) on January 4, 2019.