蛋白激酶C抑制剂对缺血/再灌注海马CAl区迟发性神经元死亡的作用研究

目的:蛋白激酶C与脑组织缺血性损害有密切关系,且证明可调节一氧化氮合成酶的活性。作为PKC抑制剂,灯盏花素可抑制蛋白激酶C的活性,但其对大鼠海马CAl区缺血/再灌注损害的作用和机制需深入研究。方法:四血管闭塞复制大鼠前脑缺血／再灌注模型,观察PKC抑制剂灯盏花素对海马CAl区NO浓度、局部脑血流量及CAl区锥体细胞密度变化的影响。结果:PKC抑制剂灯盏花素对大鼠海马CAl区缺血／再灌注脑组织的作用为降低CAl区局部NO的产生、明显改善脑组织的rCBF和显著降低该区锥体细胞的脱失。结论:PKC抑制剂对大鼠前脑缺血／再灌注所致海马CAl区迟发性神经元死亡的保护作用与其降低局部NO的产生及增加局部脑血流量有密切关系。

Experimental research of PKC inhibitor on delayed neuronal death of the rat hippocampus Cal region after transient forebrain ischemia/reperfusion

Objective: Protein kinase C (PKC) was considered to have an important role in the cerebral ischemic/reper fusional damage, and a regulating role to the nitric oxide synthase . The eregeron breviscapus can inhibite the PKC activity, but its role and machanism in the cerebral ischemia/ reperfusion were needed to explore. Methods: The animal models of the forebram ischemia/reperfusion was established in male Wistar rats. The nitric oxide (NO)concentration, regional cerebral blood flow (rCBF) and neuronal density in CA1 region of hippocampus were measured. Results: PKC inhibiyor e rigeron breviscapus increased rCBF, decreased NO concentration and delayed neuronal death in CA1 region of hippocampus. Conclustion: This study shown that the PKC inhibitor erigeron breviscapus can improve rCBF and decreased NO producing and suggested that PKC inhibitor may really have a protective effect on neurons in CA1 region of hippocampus.