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AIM: To investigate the neuroprotective effect of GZ-02 onanoxia and acute cerebral ischemia mice and focal cerebralischemia in rats and compare it with that of 3-n-butylphthalide(NBP). METHODS: Anoxia was produced by closenomobaric hypoxia; acute cerebral ischemia was produced bypermanent occlusion of the proximal of the left middle cerebralartery (MCAO). The infarct area was measured by 2, 3, 5-triphenyltetrazolium chloride (TTC) staining technique. Theextent of neurological deficit was evaluated by the method of
AIM: To investigate the neuroprotective effect of GZ-02 onanoxia and acute cerebral ischemia mice and focal cerebral ischemia in rats and compare it with that of 3-n-butylphthalide (NBP). METHODS: Anoxia was produced by closenomobaric hypoxia; acute cerebral ischemia was produced by permanent occlusion of the proximal of the left middle cerebralartery (MCAO). The infarct area was measured by 2, 3, 5-triphenyltetrazolium chloride (TTC) staining technique. Theextent of neurological deficit was evaluated by the method of