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目的 探讨血小板活化因子 (PAF)在缺血性脑损伤中的作用机制。方法 大鼠全脑缺血再灌注后 ,分别应用放免法和 Fura- 2 / AM荧光法测定海马组织中 PAF、突触体游离钙 ([Ca2 + ]i)浓度。结果 缺血 2 0 min后 ,PAF含量显著高于对照组 ,再灌注 2 40 m in时已降至对照组水平 ,再灌注 480 m in后出现迟发性升高。对应 [Ca2 + ]i值随所观察的再灌注时间延长而增加。 Tetrandrine(钙拮抗剂 )能明显降低再灌注 480 min时 PAF和 [Ca2 + ]i水平。结论 全脑缺血再灌注后 ,PAF的异常代谢与 [Ca2 + ]i水平密切关联 ,协同参与了神经细胞损伤的发生及发展。
Objective To investigate the mechanism of action of platelet activating factor (PAF) in ischemic brain injury. Methods After global cerebral ischemia and reperfusion, the levels of PAF and synaptosomal calcium ([Ca2 +] i) in hippocampus were detected by radioimmunoassay and Fura-2 / AM fluorescence assay respectively. Results After 20 min of ischemia, the PAF level was significantly higher than that of the control group. The level of PAF decreased to the level of control group after 240 min of reperfusion, and delayed after 480 min of reperfusion. The corresponding [Ca2 +] i value increased with the observed reperfusion time. Tetrandrine (calcium antagonist) significantly reduced PAF and [Ca2 +] i levels at 480 min after reperfusion. Conclusion The abnormal metabolism of PAF is closely related to the level of [Ca2 +] i after global cerebral ischemia-reperfusion, and it is involved in the occurrence and development of nerve cell injury.