ABSTRACT
Objective:To investigate the content change of EGF and NT-4/5 in the the frontal lobe,hippocampus and thalamus of rats after cerebral ischemia-reperfusion,in order to reveal the dynamic protection of EGF and NT-4/5 to cerebellum ischemia-reperfusion injury.Methods:Wistar senile rats were divided into the control group and the experiment groups at random.The control group included 5.The experimental groups were divided into cerebral ischemia 15 min group and ischemia-reperfusion 1 h,6 h,2 d,4 d,9 d groups after 15 min ischemia,5 rats per group.Results:There was all a little expression of EGF and NT-4/5 in the frontal lobe,hippocampus and thalamus of normal senile rats.The frontal lobe was shown evident increase of EGF expression in ischemia-reperfusion 2 d only.The hippocampus was shown continued increase of EGF expression during ischemia-reperfusion 6 h to 4 d and the EGF expression was shown a peak in ischemia-reperfusion 4 d.The increase of EGF expression in thalamus continued during ischemia-reperfusion 2-9 d too.The NT-4/5 expression of the frontal brain was clearly reduced after ischemia-reperfusion and returned to normal in ischemia-reperfusion 9 d.The NT-4/5 expression of hippocampus was shown one-off reduction after ischemia-reperfusion,but the expression quickly returned to normal and shows a little increase.The thalamus had only one-off reduction of NT-4/5 expression.Conclusion:The frontal lobe lacks of fast neuroprotective mechanism of EGF in early stage of ischemia-reperfusion and it has a limited neuroprotective effect of EGF in middle and advanced stage.The hippocampus has a fast and long-lasting neuroprotective mechanism of EGF.The thalamus has a delayed neuroprotective mechanism of EGF.The frontal brain and hippocampus have a delayed neuroprotective mechanism of NT-4/5.The neuroprotective mechanism of NT-4/5 is weaker in thalamus.
ABSTRACT
OBJECTIVES: We examined the effects of neurotrophins and insulin-like growth factors on cell death induced by haloperidol, a typical anti-psychotic agent. METHOD: Neocortices from 14- or 15-daysold fetal mice for neuron-glia co-cultures were used for this experiment. RESULT: Twenty-four hours treatment of mouse cortical cell cultures with 30 M haloperidol-induced wide spread neuronal apoptosis characterized by cell body shrinkage, DNA fragmentation and condensation. Concurrent treatment with growth factors, BDNF, NT4/5, IGF-I and IGF-II, protect the neurons from the haloperidol-induced neuronal apoptosis(HINA) in a dose dependent manner(10-100ng/ml). CONCLUSION: The present study suggests the possibility that haloperidol toxicity can be hampered with growth factors. Further study about the mechanism underlying the protective capacity of the growth factors on HINA may lead to the development of the new protective strategy for tardive dyskinesia.