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目的 研究大鼠全脑缺血再灌注损伤后酪氨酸羟化酶 (TH)和多巴胺 β 羟化酶 (DβH)表达的改变及意义。方法 利用改良四血管闭塞法 ,建立大鼠全脑缺血模型。于缺血再灌注后 1,3,5d断头取脑 ,行免疫组化染色 ,在光镜下观察海马CA1区神经元TH及DβH表达的变化 ,并计数海马CA1区正常神经元。结果 全脑缺血再灌注后 1d ,TH及DβH的表达呈阴性 ,海马CA1区神经元未见显著的病理形态学改变 ;全脑缺血再灌注后 3d ,TH及DβH呈阳性表达 ,海马CA1区可见部分神经元死亡 ;全脑缺血再灌注后 5d ,TH及DβH呈明显阳性表达 ,海马CA1区可见大部分神经元死亡。结论 全脑缺血再灌注后 ,由于TH及DβH异常表达 ,使得儿茶酚胺生物合成增加 ,这可能是短暂性脑缺血损伤的机理之一。
Objective To investigate the changes of tyrosine hydroxylase (TH) and dopamine β hydroxylase (DβH) after global cerebral ischemia-reperfusion injury in rats and its significance. Methods The model of global cerebral ischemia was established by modified four vessel occlusion. The brain was decapitated at 1, 3 and 5 days after ischemia-reperfusion. The expression of TH and DβH in hippocampal CA1 neurons was observed under light microscope. The normal neurons in CA1 hippocampus were counted. Results The expression of TH and DβH was negative on the 1st day after global cerebral ischemia-reperfusion. The neurons in CA1 area of the hippocampus had no significant pathological changes. The levels of TH and DβH were positive on the 3rd day after global cerebral ischemia-reperfusion, The death of some neurons was observed in the area. The expression of TH and DβH was significantly positive on the 5th day after global cerebral ischemia and ischemia, and most of the neurons died in CA1 area of hippocampus. Conclusion After global cerebral ischemia and reperfusion, the abnormal expression of TH and DβH leads to increased catecholamine biosynthesis, which may be one of the mechanisms of transient ischemic injury.