Postconditioning has regenerated interest as a mechanical intervention against cerebral
ischemia/reperfusion injury, but its molecular mechanisms remain unknown. We previously …

Psychostimulants alter gene expression in projection neurons of the striatum, and such
neuroplasticity is implicated in drug addiction and dependence. Evidence indicates that …

J. Neurochem. (2010) 114, 897–908. Abstract It is well established that pre‐conditioning
protects neuronal injury against ischemia. However, the molecular mechanisms underlying …

Hypoxia administered after transient global cerebral ischemia (tGCI) has been shown to
induce neuroprotection in adult rats, but the underlying mechanisms for this protection are …

2′,2′,3′,3′,4′,4′,5′,5′,6′,6′,-decabrominated diphenyl ether (PBDE-209) is the
most widely used polybrominated diphenyl ethers (PBDEs) globally. Some animal …

Mitophagy alleviates neuronal damage after cerebral ischemia by selectively removing
dysfunctional mitochondria. Phosphatase and tensin homolog (PTEN) induced putative kinase 1 (…

Autophagy disruption leads to neuronal damage in hypoxic–ischemic brain injury. Rab7, a
member of the Rab GTPase superfamily, has a unique role in the regulation of autophagy. …

Ischemic postconditioning, a series of mechanical interruptions of blood flow immediately
after reperfusion, has been described in brain studies. However, hypoxic postconditioning (…

Our previous data indicated that hypoxic preconditioning (HPC) ameliorates transient global
cerebral ischemia (tGCI)-induced neuronal death in hippocampal CA1 subregion of adult …

Hypoxic postconditioning (HPC) is an innovative neuroprotective strategy with cytoprotective
effects on the hippocampal neurons against transient global cerebral ischemia (tGCI) in …