Neurological research
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Neurological research · May 2012
Activation of Akt/GSK-3beta/beta-catenin signaling pathway is involved in survival of neurons after traumatic brain injury in rats.
Apoptotic cell death is an important factor influencing the prognosis after traumatic brain injury (TBI). Akt/GSK-3beta/beta-catenin signaling plays a critical role in the apoptosis of neurons in several models of neurodegeneration. The goal of this study was to determine if the mechanism of cell survival mediated by the Akt/GSK-3beta/beta-catenin pathway is involved in a rat model of TBI. ⋯ Phosphorylation of Akt (Ser473) and GSK3beta (Ser9) was accelerated in the injured cortex, and involved in the neuronal survival after TBI. Moreover, neuroprotection of beta-catenin against ischemia was partly mediated by enhanced and persistent activation of the Akt/GSK3beta signaling pathway.
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Neurological research · May 2012
ReviewNeuroprotection targeting ischemic penumbra and beyond for the treatment of ischemic stroke.
Neuroprotection to attenuate or block the ischemic cascade and salvage neuronal damage has been extensively explored for the treatment of ischemic stroke. In the last two decades, neuroprotective strategy has been evolving from targeting a signal pathway in neurons to protecting all neurovascular components and improving cell-cell and cell-extracellular matrix interaction that ultimately benefits the brain recovery after ischemic stroke. The progression from potentially reversible to irreversible injury in the ischemic penumbra has provided the opportunity to develop therapies to attenuate the ischemic stroke damage. ⋯ In addition, increasing evidence has indicated ischemic stroke could induce long-lasing cellular and hemodynamic changes beyond the ischemic territory. It is unclear whether and how the global responses induced by the ischemic cascade contribute to the progression of cognitive impairment after ischemic stroke. The prolonged pathophysiological cascades induced by ischemic stroke beyond the ischemic penumbra might provide novel therapeutic opportunities for the neuroprotective intervention, which could prevent or slow down the progression of vascular dementia after ischemic stroke.
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Neurological research · May 2012
Changes in spinal cord met-enkephalin levels and mechanical threshold values of pain after pulsed radio frequency in a spared nerve injury rat model.
The present study investigated changes in the met-enkephalin (M-ENK) levels in the spinal cord. We also determined the mechanical threshold value of pain in spared nerve injury (SNI) rats after applying pulsed radiofrequency (PRF) on L5 dorsal root ganglion (DRG). ⋯ This study demonstrates that applying PRF on the DRG can improve hyperalgesia and increase M-ENK levels in the spinal cord of SNI rats within 24 hours. These findings indicate that the endogenous M-ENK in the spinal cord is involved in the mechanism of PRF on the therapy of neuropathic pain.