Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuronal damage and axonal regeneration inhibition are the main reasons to poor functional recovery after ischemia. Nogo-A signals inhibit axon outgrowth through the PirB receptor after ischemic reperfusion injury in central nervous system. We use TAT-PEP, a novel protein which could pass through the blood brain barrier, to block the function of PirB and identify the long-term neurological and behavioral recovery after bilateral common carotid artery occlusion (BCCAO) in mice. We observed that TAT-PEP promoted neuron survival and inhibited neuronal apoptosis. TAT-PEP increased the expression of Tau, GAP43 and MAP-2 proteins. In addition, the short-term and long-term cognitive functions were also enhanced, indicating that TAT-PEP had a long-term neuroprotective effect, which reduced neurologic injury and neuron loss, promoted neurite outgrowth and enhanced functional recovery after ischemia. These studies reveal the mechanism of PirB on stroke and offer a potential therapeutic method for cerebral ischemia in humans.
 ...
PMID:TAT-PEP, a novel blocker of PirB, enhances the recovery of cognitive function in mice after transient global cerebral ischemia. 2831 58

The memory dysfunction is one of the disastrous outcomes for perinatal hypoxia ischemia. Erythropoietin (EPO) has been demonstrated as a neuroprotective agent with multiple effects in a series of neurological diseases. We hypothesized that disruption of neural network including synapses and neurites would contribute to memory dysfunction induced by hypoxia ischemia. The aim of the present study was to elucidate the involvement of EPO on synaptogenesis and neurite repair following perinatal hypoxia ischemia. Using a neonatal hypoxia ischemia rat model, we found that EPO rescued hypoxia ischemia-induced decrease of synaptic proteins including Synapsin1 and PSD95 rather than GluR1 in the cortex and hippocampus. In addition, EPO reduced the expression of APP (an axonal injury marker), induced the expression of microtubule-associated protein MAP-2 (a dendritic marker), and restored axonal density after hypoxia ischemia. These changes contributed to improving electrophysiological properties of synapses and spatial memory performance. In summary, our data revealed an important role of EPO in synaptogenesis and neurite repair, providing a new insight into cellular mechanisms underlying cognitive and memory dysfunction associated with perinatal hypoxia ischemia.
 ...
PMID:Erythropoietin induces synaptogenesis and neurite repair after hypoxia ischemia-mediated brain injury in neonatal rats. 3126 Dec 38


<< Previous 1 2 3 4