Acs Chem Neurosci
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The recent coronavirus disease of 2019 (COVID-19) pandemic has adversely affected people worldwide. A growing body of literature suggests the neurological complications and manifestations in response to COVID-19 infection. ⋯ Our findings demonstrated a surge in the number of reactive astrocytes and activated microglia, as well as low levels of glutathione along with the upregulation of inflammation- and immune-related genes IL1B, IL6, IFITM, MX1, and OAS2 in the COVID-19 group. Overall, the data imply that oxidative stress may invoke a glial-mediated neuroinflammation, which ultimately leads to neuronal cell death in the cerebral cortex of COVID-19 patients.
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Cerebral ischemia-reperfusion injury (CIRI) mainly arises from the clinical treatment of ischemic stroke, induced by the blood-brain barrier (BBB) disruption and infiltrated inflammation. The Sigma-1 receptor (Sigma-1R) is a novel target for neuroprotection, and the α2-receptor agonist pain medication dexmedetomidine displays a neuroprotective effect through activating Sigma-1R. The present study aims to investigate the potential therapeutic effect of dexmedetomidine in a mouse stroke model and hypoxia/reoxygenation(OGD/R)-induced brain endothelial dysfunction. ⋯ Moreover, blockage of Sigma-1R by its antagonist BD1047 abolished the neuroprotective property of dexmedetomidine in both animal and cell culture experiments. On the basis of these findings, we conclude that dexmedetomidine therapy shows neuroprotection in MCAO mice. Mechanistically, dexmedetomidine alleviated hypoxia/reoxygenation-induced cerebral endothelial dysfunction by activating the Sigma-1R-mediated signaling pathway.