Study Of The Effects Of Hypothermia On Apoptosis And The Activation Of Caspase-3 Following Transient Forebrain Ischemia

[Objective]To explore the neuroprotective mechanism of mild hypothermia by studying the effects of mild hypothermia on apoptosis and the activation of caspase-3 following transient forebrain ischemia. [Methods]Transient forebrain ischemia was carried out in rats with Smith's model modified by Chan.The model was made by llmin of bilateral common carotid artery occlusion and hypotension in rat.The neuronal absence in the CAi section of hippocampus was observed by nissel body stain.Apoptosis was dectected by in situ end-labeling of fragmente DNA.Immunhistochemistry was used to detecte the activation of caspase-3. [Results]1. The hippocampal CAj neurons in normothemic group(NT) were remarkably absent compared with control group.2. The apoptotic neurons in hippocampal CAi section were observed in normothermic and hypothermic ischemia groups,and the quantity of apoptotic neurons in mild hypothermic ischemia was less than that of normothermic group(P<0.01).3. The positive caspase-3 immunostain was dectected in the hippocampal CAi pyramidal cells in the normothennic and hypothermic group 48h after cerebral ischemia, but not in the the central group. [Conclusions]The model of transient forebrain cerebral ischemia made by 11 min of bilateral common carotid artery occlusion and hypotension in rats was sucessful. This model was simplicity,good duplicability and consistency. The neuroprotection of hypothermia was confirmed with this model. The delayed neuronal deaths after transient forebrain ischemia was via apoptosis.The activation of caspase-3 is a critical step in apoptosis. It was assumed that mild hypothermia can protect neurons through decreasing apoptosis.