Abstract
Neuroprotective therapy is crucial to salvage the penumbra surrounding the core of ischemia in the acute phase of ischemic stroke. Cumulative evidence suggests that apoptosis plays a pivotal role in neuronal cell death after cerebral ischemia in various experimental animal models. The time-dependent molecular and biochemical sequelae that lead to apoptotic cell death after the interruption of cerebral blood flow have been established. Therefore, various kinds of neuroprotective agents have been developed.
In this symposium we introduced the ischemic cell death pathway, especially intrinsic mitochondriadependent and extrinsic receptor-mediated pathway of apoptosis after ischemia, and also introduced our experimental studies on several kinds of brand-new neuroprotective compounds after focal ischemia. Moreover, extra-mild hypothermic therapy (35°C) enhanced that neuroprotective effect and prolonged that therapeutic time window, was introduced.°C
These present data show that these newly developed neuroprotective agents and the combination treatment with extra-mild hypothermia (35°C) are effective for neuroprotection in acute cerebral ischemia. These studies provide an impetus for novel therapeutic targets in neuroprotective strategies in acute ischemic stroke. These combined therapy may be useful in clinical medical care for acute ischemic stroke in human.
