Abstract
There is increased evidence supporting the contribution of oxidative stress to ischemia/reperfusion-induced damage in a consecutive two-phase pattern : immediate direct cytotoxic effects and subsequent redox-mediated inflammatory injury. It is thought that research into the pleiotropic effects of several drugs would be a useful strategy for the development of new brain protective therapies. From this perspective, we have attempted to evaluate the potential brain protective effects of several drugs.
Cognitive impairment, swallowing disturbance, and depression are crucial complications causing specifically attributable proportions of disability in patients with stroke. We established an animal model by permanent occlusion of both common carotid arteries causing chronic cerebral ischemia, and assessed the effect of several drugs.
Recently, a few reports have indicated that type III phosphodiesterase inhibitor (PDE III-1), which is clinically used for the treatment of chronic cerebral infarction as an anti-platelet agent, has neuroprotective effects. We assessed the neuroprotective mechanisms of PDE III-I through signaling pathways, which lead to the activation of cyclic adenosine monophosphate (cAMP) responsive element binding protein (CREB) phosphorylation using this chronic cerebral hypoperfusion model.
In the future, we expect that the clinical utility of new brain protective agents will be developed based on a multi-target mechanism.
