Neuroprotection by baicalein in ischemic brain injury involves PTEN/AKT pathway.

摘要: J. Neurochem. (2010) 112, 1500–1512. Abstract Recently more evidences support baicalein (Bai) is neuroprotective in models of ischemic stroke. This study was conducted to determine the molecular mechanisms involved this effect. Either permanent or transient (2 h) middle cerebral artery occlusion (MCAO) induced rats study. Permanent MCAO led larger infarct volumes contrast MCAO. Only MCAO, Bai administration significantly reduced size. Baicalein also markedly apoptosis penumbra rats. Additionally, oxygen and glucose deprivation (OGD) used mimic insult primary cultured cortical neurons. A rapid increase intracellular reactive species level nitrotyrosine formation by OGD counteracted Bai, which parallel with attenuated cell injury. The reduction phosphorylation Akt glycogen synthase kinase-3β (GSK3β) restored associated preserved levels PTEN, phophatase that negatively regulates Akt. As a consequence, Bcl-2/Bcl-xL-associated death protein increased Bcl-2 motochondria maintained, subsequently antagonize cytochrome c released cytosol. LY294002 blocked phospho-AKT evoked abolished protective Together, these findings provide evidence protects neurons against ischemia injury effect involves PI3K/Akt PTEN pathway.