Jieqiong Gao

TL;DR: Autophagy was activated in the reperfusion phase, as revealed in both mice with middle cerebral artery occlusion and oxygen-glucose deprived cortical neurons in culture, and the protective role of autophagy during reperfusions may be attributable to mitophagy-related mitochondrial clearance and inhibition of downstream apoptosis.

TL;DR: It is demonstrated that the ER stress induced by tunicamycin and thapsigargin protects against the transient ischemic brain injury, and the PARK2-mediated mitophagy may be underlying the protection of ER stress.

TL;DR: H3R promotes I/R injury while its antagonism protects against ischaemic injury via histamine-independent mechanisms that involve suppressing H3R/CLIC4 binding-activated autophagy, suggesting that H3 R inhibition is a therapeutic target for cerebral ischaemia.

TL;DR: Results indicate that histamine can effectively protect against OGD-induced cell damage in astrocytes through H1 and H2 receptors, and its regulatory effect onAstrocytic GS expression may be due to the activation of H1 receptor and PKC pathway.

TL;DR: Carnosine may be an endogenous regulator of astrocyte energy metabolism and a clinically safe therapeutic agent for promoting brain energy metabolism recovery after ischemia/reperfusion injury.