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目的:探讨姜黄素(curcumin)对癫痫大鼠认知功能障碍的预防作用及其可能机制。方法:将30只成年雄性SD大鼠分为正常对照组、单纯致痫组(SE组)、姜黄素[60mg/(kg.d)]干预组(curcumin组)。采用Morris水迷宫方法检测大鼠学习记忆功能变化,并检测脑片水平的长时程增强(LTP)变化,处死大鼠后取脑组织并匀浆,测超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、谷胱甘肽(GSH)、丙二醛(MDA)的水平。结果:(1)SE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SE组显著缩短(P<0.05)。撤离平台后,SE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),姜黄素治疗后大鼠在平台所在象限的停留时间较SE组显著延长(P<0.05)。(2)给予HFS刺激后各组兴奋性突出后电位(fEPSP)斜率较前明显增加,均可持续1h以上,与对照组比较SE组HFS刺激后fEPSP斜率明显减小(P<0.05),姜黄素可减轻SE所致的fEPSP斜率减小(P<0.05)。(3)SE组SOD、GSH-PX、GSH显著下降,MDA明显增高,姜黄素可逆转上述现象,有统计学意义(P<0.05)。结论:姜黄素可显著减轻癫痫持续状态所致的大鼠认知功能障碍,减轻海马区的氧化应激反应从而保护海马海马是其可能机制之一。
Objective: To investigate the preventive effect of curcumin on cognitive dysfunction in epileptic rats and its possible mechanism. Methods: Thirty adult male Sprague-Dawley rats were divided into normal control group, epilepsy group (SE group) and curcumin group (curcumin group) [60mg / (kg · d)]. Morris water maze method was used to detect the changes of learning and memory function in rats, and the changes of long-term potentiation (LTP) in brain slices were detected. The rats were sacrificed and the brain tissue was taken out and homogenized. The activity of superoxide dismutase (SOD) (GSH-PX), glutathione (GSH), and malondialdehyde (MDA) levels were measured. Results: (1) The latent period of looking for platform in SE group was significantly longer than that in control group (P <0.05). The incubation period for finding platform in curcumin group was significantly shorter than SE group (P <0.05). After evacuation of the platform, the residence time of rats in SE group was significantly shorter than that of the control group (P <0.05). The retention time of curcumin in the quadrant of the platform was significantly longer than that in SE group (P <0.05). (2) After the stimulation of HFS, the slope of fEPSP in each group increased significantly compared with that of the previous group, and the slope of fEPSP in SE group was significantly lower than that of the control group (P <0.05) Supranoside reduced the slope of fEPSP induced by SE (P <0.05). (3) The levels of SOD, GSH-PX and GSH in SE group decreased significantly and MDA significantly increased. Curcumin could reverse the above phenomenon, with statistical significance (P <0.05). Conclusion: Curcumin can significantly reduce cognitive impairment in rats induced by status epilepticus, reduce the oxidative stress response in hippocampus and protect the hippocampus, which may be one of the possible mechanisms.