Cerebral ischemia-reperfusion injury plays an important role in the evolution of brain damage through mechanisms that include the generation of reactive oxygen species(ROS),oxidative stress,inflammati
Background Adult cortex has long been regarded as “non-neurogenic”.Recent studies have indicated the occurrence of neurogenesis in cortex after ischemic stroke.
To explore the dynamic change of interleukin-17A(IL-17A)in cerebrospinal fluid(CSF)and blood after ischemic stroke in vivo.Futher,to observe whether there are some nerve cells involved in the secretio
Objective Hippocampus is one of the most vulnerable regions after ischemic stroke.Until now the mechanism of ischemia-reperfusion injury has not been understood clearly.
To investigate the neuroprotective effects of neurotrophin-3(NT-3) expression controlled by five copies of the hypoxia-responsive elements(5HRE)after focal cerebral ischemia.
Our previous study has proved that the up-regulation of glial glutamate transporter 1(GLT-1)induced by cerebral ischemic preconditioning(CIP)played an important role in the acquisition of brain ischem
Neuregulin receptor degradation protein-1(Nrdp1)is an E3 ubiquitin ligase that regulates the proteasomal degradation and activity of proteins involved in cell growth,inflammation and apoptosis,includi
As a therapeutic strategy,remote ischemic postconditioning holds great promise for ischemic stroke,but the underlying mechanisms yet remain unclear,hindering its translation from bench to beside.
MicroRNA-99a(miR-99a) has been reported to function as a tumor suppressor through regulating cell cycle and apoptosis.But its clinical significance in ischemic stroke and its function in cerebral isch