姜黄素预防高原缺氧大鼠认知功能障碍的机制研究

Curcumin prevents hypobaric hypoxia-induced cognitive deficits in rats:a mechanism study

目的探讨姜黄素(Curcumin)预防高原缺氧大鼠认知功能障碍的机制。方法将24只成年雄性SD大鼠随机分为健康对照组、模型组(model组)、姜黄素[按体重60 mg/(kg.d)]防治组(curcumin组)。造模后,给予姜黄素防治,采用Morris水迷宫实验方法检测各组大鼠学习记忆功能变化,并运用Western blot技术检测海马Bcl-2、Bax及活化的caspase-3等凋亡相关蛋白表达水平的变化。结果①模型组大鼠寻找平台的潜伏期明显长于对照组,具有统计学意义(P<0.05),姜黄素组寻找平台的潜伏期相对于模型组显著缩短(P<0.05)。撤离平台后,模型组大鼠在平台所在象限的停留时间明显短于对照组(P<0.05),姜黄素干预后大鼠在平台所在象限的停留时间较模型组显著延长(P<0.05);②姜黄素可显著减轻慢性缺氧导致的Bax、活化的caspase-3表达水平升高级Bcl-2表达水平下降。结论姜黄素可显著改善高原缺氧大鼠认知功能障碍,其机制可能和减轻海马神经元的凋亡有关。

Objective To investigate the mechanism of curcumin preventing hypobaric hypoxia-induced cognitive deficits in rats. Methods A total of 24 male Sprague-Dawley rats （20020）g were randomly divided into three groups with 10 rats in each： control group, model group and curcumin group. Severe cognitive deficits were detected by the water maze test. Expressions of Bcl-2, Bax and active caspase-3 protein in the hippocampus of rats were detected by Western blotting. Results Hypobaric hypoxia can cause severe cognitive deficits, and curcumin could attenuate hypobafic hypoxia-induced cognitive deficits in rats. Curcumin inhibited the activation of caspase-3 and prevented the increase of ax/Bcl-2 ratio in the hippocampns. Condusion Curcumin can attenuate the cognitive deficits caused by chronic cerebral hypoperfusion and it might be associated with the apoptosis decrease of hippocampal neurons.