• Likai Shi, Baowei Li, Guoqing Chen, Yingsi Huang, Zhenpu Tian, Lifeng Zhang, Li Tian, and Qiang Fu.
• Department of Anesthesiology, The First Medical Center of the Chinese People's Liberation Army (PLA) General Hospital, No. 28 Fuxing Road, Beijing, China.
• Shock. 2022 Jan 1; 57 (1): 118130118-130.

ObjectiveMicroglial activation is a vital process in the neuroinflammatory response induced by I/R injury. It has been reported that myocyte enhancer factor (MEF)2D expression in activated microglia is associated with microglia-induced inflammatory responses and plays an important role in neuronal survival. This research aimed to investigate the role and mechanism of MEF2D in microglial activation and neuroinflammation in cerebral I/R in vitro and in vivo.MethodsA cerebral I/R model was established. In vitro, neuronal, or microglial cells were exposed to oxygen-glucose deprivation and reoxygenation to mimic I/R. MEF2D overexpression was induced, and siRNA was administered in vitro and in vivo. Microglial polarization; MEF2D, nuclear transcription factor (NF)-κb, TLR4, and cytokine levels; neuronal injury; mitochondrial function; brain injury and cognitive function were detected in the different groups in vitro and in vivo.ResultsWe found that oxygen-glucose deprivation increased MEF2D expression in a time-dependent manner in BV2 cells and primary microglia. MEF2D overexpression inhibited microglial activation, the expression of NF-κb and TLR, cytokine levels, and neuronal injury in microglia exposed to oxygen-glucose deprivation and reoxygenation. In the middle cerebral artery occlusion model, microglial activation, the neuroinflammatory response, mitochondrial dysfunction, brain injury, and cognitive function were improved by MEF2D overexpression and aggravated by MEF2D siRNA treatment.ConclusionThese results indicate that MEF2D is a necessary molecule for neuroinflammation regulation and neuronal injury in cerebral ischemia.Copyright © 2021 by the Shock Society.

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