鼠大脑局灶缺血神经元凋亡及其防治的研究
基本信息
结项摘要
本项目采用Wistar大鼠全脑及局灶缺血/再灌流及神经元培养缺血模型，用分子生物学、免疫组化等技术观察缺血/再灌流以后蛋白激酶C活性、神经元内游离钙、Caspase-3、c-fos、bcl-2表达及神经元凋亡的变化，同时观察了蛋白激酶C抑制剂对上述指标的影响。结果发现脑缺血/再灌流可以诱导神经元蛋白激酶C的移位激活、神经元钙超载、c-fox、bcl-2及Caspase-3表达增加及神经元凋亡增加，蛋白激酶C抑制剂可以防止上述变化。结果提示脑缺血/再灌流可诱导神经元蛋白激酶C的移位激活，蛋白激酶C的移位激活参与神经元凋亡的发生。蛋白激C激活参与神经元凋亡的发生与①促进钙超载；②促进NOS表达；③促进c-fos表达；④促进Caspase-3级联反应的信号通路有关。
项目摘要
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数据更新时间：2023-05-31
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