论文部分内容阅读
目的观察缺血预处理对脑皮质缺血再灌注期间神经元凋亡及磷酸化糖原合酶激酶-3β(GSK-3β)的影响,探讨其保护作用机制。结论雄性Wistar大鼠30只,随机分为假手术组(S)、缺血再灌注组(I/R)及预处理组(IPC),每组各10只。采用4-VO法建立大鼠全脑缺血再灌注模型。IPC组分离双侧颈总动脉,夹闭10s,开放30s,反复3次,最后夹闭10min。于术后2d处死大鼠,取出脑组织,采用TUNEL法检测大鼠皮质神经元凋亡情况;TTC法检测大鼠脑部梗死面积;光谱法检测磷酸化的GSK-3β水平(p-GSK-3β);采用Linear Regression分析GSK-3β活性与大鼠皮质神经元凋亡、脑部梗死面积的相关性。结果与S组相比,I/R组和IPC组皮质神经元凋亡和梗死面积显著增多(P<0.01),p-GSK-3β水平降低(P<0.01);与I/R组相比,IPC组皮质神经元凋亡和梗死面积显著减少(P<0.01),p-GSK-3β水平增高(P<0.01);p-GSK-3β与大鼠皮质神经元凋亡、脑部梗死面积之间具有高度相关性(P<0.01)。结论缺血预处理使p-GSK-3β水平增高,脑皮质神经元凋亡和梗死面积减少,从而减轻脑缺血再灌注损伤。
Objective To observe the effect of ischemic preconditioning on neuronal apoptosis and phosphorylation of glycogen synthase kinase-3β (GSK-3β) during cerebral ischemia / reperfusion in rats and its protective mechanism. CONCLUSION: Thirty male Wistar rats were randomly divided into sham operation group (S), ischemia reperfusion group (I / R) and preconditioning group (IPC), with 10 rats in each group. Rat model of global cerebral ischemia-reperfusion was established by 4-VO method. IPC group separated from the common carotid artery, clamping 10s, open 30s, repeated 3 times, and finally clipped 10min. The rats were sacrificed at 2 days after operation and the brain tissue was removed. The apoptosis of cortical neurons was detected by TUNEL method. The area of cerebral infarction was detected by TTC method. The phosphorylation level of GSK-3β (p-GSK- 3β). The correlation between GSK-3βactivity and cortical neuron apoptosis and infarct size was analyzed by Linear Regression. Results Compared with S group, the apoptosis and infarct size of cortical neurons in I / R group and IPC group were significantly increased (P <0.01) and the level of p-GSK-3β was decreased (P <0.01). Compared with I / R group (P <0.01). The level of p-GSK-3β was increased in IPC group (P <0.01). The effect of p-GSK-3β on the apoptosis of cerebral cortex neurons and infarction area There was a high degree of correlation (P <0.01). Conclusion Ischemic preconditioning increases the level of p-GSK-3β, decreases the apoptosis of cerebral cortex neurons and the area of infarction, thus alleviates cerebral ischemia-reperfusion injury.