高温下蛋白激酶对海马神经元细胞保护作用
Effect of protein kinase C on hippocampal neurons apoptosis induced by hyperthermia
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摘要:目的 探讨蛋白激酶C(PKC)在高温诱导海马神经细胞凋亡中的作用, 为防治高温致脑损伤提供实验依据。方法 通过建立体外高温诱导海马神经细胞原代培养的凋亡模型, 应用PKC特异性抑制剂氯化百屈菜红碱(chelery thrine chloride), 观察海马神经元胞内Ca2+浓度的动态变化以及对B淋巴细胞瘤基因2蛋白(Bcl-2)表达的影响。结果 42℃处理1h, 加入蛋白激酶抑制剂氯化百屈菜红碱(CTC)后, 海马神经细胞内Ca2+浓度迅速明显上升, 25~30s即达峰值, 尔后平缓下降, 并维持于高于原来基线的水平; 免疫组织化学结果显示处理后海马神经细胞内Bcl-2表达较单纯42℃处理1h后表达明显下降。结论 CTC对高温作用后海马神经元胞内Ca2+浓度和Bcl-2表达具有重要的影响, 说明PKC激活在高温诱导的海马神经细胞凋亡中具有重要的保护作用。Abstract:Objective To investigate the effect of protein kinase C on the hippocampus neurons apoptosis induced by hy perthermia and to provide the evidence for the prevention of brain injuries caused by hyperthermia.Methods By establishing the apoptosis model of primary culture of hippocampal neurons induced by hy perthermia, the dynamic change of concentration of Ca2+ in hippocampal neurons and the influence to Bcl-2 expression were observed after using chelerythr ine chloride(CTC) which was the special inhibitor of PK C.Results The concentration of Ca2+ in hippo campal neurons increased rapidly with hyperthermia treatment(42)for 1 h and application of CTC.The climax of increase was arrived after 25~30 s, and de creased slowly until to keep the higher level than that of normal level.The expression of Bcl-2 in hippocampal neurons with hyperthermia and CTC treatment decreased dist inctly more than that of cells in 42 for 1 h.Conclusion The activation of PKC played a very important protection role in the apoptosis induced by hyperthermia in hippocampal neurons.The application of CTC influenced greatly the concentration of Ca2+ and the expression of Bcl-2 in hippocampal neurons after hyperthermia.
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