Se-(Methyl)-selenocysteine ameliorates blood-brain barrier disruption of focal cerebral ischemia mice via ferroptosis inhibition and tight junction upregulation in an Akt/GSK3 β-dependent manner

ConclusionThese results suggested that SeMC exerted protection against ischemic stroke, which might be attributed to activating the Akt/GSK3 β signaling pathway and increasing the nuclear translocation of Nrf2 and β-catenin, subsequently maintaining the integrity of BBB.Graphical abstract
Source: Psychopharmacology - Category: Psychiatry Source Type: research