| Objective: The aim of this study was to observe the protective effect of Naloxone on the neural apoptosis after global cerebral ischemia-reperfusion injury in rats and provided experiment basis for the treatment of ischemia-reperfusion with Naloxone. In 1960 Jennings proposed the concept of ischemia-reperfusion injury. It was confirmed that ischemia- reperfusion injury may occur in many tissue and organs of animals and human by the clinical observation and the animal experiments .Therefore, exploring the mechanism and feature of ischemia-reperfusion injury is important to reduce injury of ischemia-reperfusion.The apoptosis played on a vital role in the nervous system .It may eliminate the unnecessarily cells and the valueless cells to guarantee the normal cells growing and maintain the internal environment stabilization. However the apoptosis not only had the positive defensive function, but also induced the occurrence of some diseases .Therefore, study on the mechanism of apoptosis process was a new way to prevent and control these diseases.At present,there are a few effective medicines which can be used for the treatment of cerebral ischemia-reperfusion injury. To seek the effective neuron protecting agent is the question which is urgently awaited to be solved in medical research. Some research found that Naloxone had therapeutic effect for the cerebral ischemia-reperfusion injury, but the mechanism is not clear completely. In our study, we try to find the relationship among Naloxone treatment and expression of Bcl-2,Bax protein as well as neuronal apoptosis after cerebral ischemia- reperfusion injury.Methods: Thirty-six male Wistar rats were used in this study. The rats weighted about 250 gram. All rats were divided into three groups at random: the sham-operated group, the control group and the treated group, the treated group were divided into four groups: 0h, 6h, 12h, 24h at the different time-spot after ischemia- reperfusion. Each group had 6 rats. Rat model of ischemia- reperfusion: anesthesia was induced with 10% chloral hydrate (350mg/kg). Four-vessel occlusion (electrical coagulating bilateral vertebral artery and ligated bilateral common carotid artery) was used to establish the model of global cerebral ischemia- reperfusion in the treated groups and control group. The artery clamps were removed to recovery reperfusion after occlusion of bilateral common carotid artery for 15 minutes. The vertebral artery were not electrically coagulated and bilateral common carotid artery were not ligated in sham-operated group, The Naloxone was injected into abdomen (2mg/kg) on the different time-spot in treated groups. Normal saline was injected into abdomen in control group. On the 48h time-spot after reperfusion all rats were killed and hippocampus was separated from the detection of apoptosis and Bcl-2, Bax protein by the Flow Cytometry (FCM).Results: The positive cell number were (3.80±0.61)% (0h group), (5.26±0.65)% (6h group), (6.35±0.45)% (12h group), (9.50±0.91)%(24h group) respectively in the treated groups. The positive cell number was by(12.32±2.72)% in the control group. There was significant difference among the treated groups and the control group (p<0.01) . The expression of Bcl-2 protein of the control group was 6.73±1.62. The means of Bcl-2 in treated groups were 9.63±1.82, 9.57±1.84, 7.30±1.31 ,6.85±1.70(0h, 6h, 12h, 24h). There was significant difference among the treated groups and the control group (p<0.01) . The expression of Bax protein of the control group was 16.97±6.37, The means of Bax in treated groups were 4.30±0.85, 5.20±1.16, 8.58±1.49, 14.88±4.07 (0h, 6h, 12h, 24h). There was significant difference among the treated groups and the control group(p<0.01) .Conclusion: The neuronal cell apoptosis may play an important role in cerebral ischemia-reperfusion injury .The Naloxone may reduce the numbers of apoptotic nervous cell. The mechanism is probably to increase the Bcl-2 protein at early time or change the ratio of Bcl-2/Bax.
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