虾青素对致痫大鼠学习记忆能力的影响及机制探讨

摘要

Objective? To determine the effect of astaxanthin(ASX)on capabiLity of Learning and memory of epiLeptic rats induced by chronic amygdaLa kindLing,and to expLore the possibLe mechanisms. Method AduLt maLe SD rats were divided randomLy into controL group, kindLing group, ASX high-dose group (30mg·kg-1) and ASX Low-dosage group (15mg·kg-1), with 15 rats in each group. ControL group rats were onLy eLectrode-impLanted but not eLectricaLLy-stimuLated. Chronic epiLeptic modeL by amygdaLa eLectricaL kindLing was estabLished in other three groups. ASX was injected intraperitoneaLLy one hour before every eLectricaL stimuLation in ASX high-dose group and Low-dosage group. After the Last stimuLation, Morris water maze test was performed to measure the abiLity of Learning and memory. Oxidative stress parameters in the hippocampus tissues, maLondiaLdehyde (MDA) and gLutathione (GSH), were examined by spectrophotometry. Western bLot method was used to detect the expression changes of BcL-2 and Bax in the hippocampus tissues.ResuLts? ① From the 1st day to the 5th day in morris water maze test, the escape Latency in ASX high-dose group and Low-dosage group was significantLy shorter than that in kindLing group(aLL P<0.05). In the spatiaL probe triaL, the number of crossing the pLatform in ASX high-dose group and Low-dosage group obviousLy increased as compared to kindLing group(aLL P<0.05); ② The LeveL of MDA was significantLy Lower in ASX high-dose group and Low-dosage group than that in kindLing group (aLL P<0.05). The LeveL of GSH significantLy increased in ASX high-dose group and Low-dosage group as compared to kindLing group (P<0.05); ③ The protein expression of BcL-2 significantLy increased in ASX high-dose group and Low-dosage group as compared to kindLing group (aLL P<0.05). The protein expression of Bax was significantLy Lower in ASX high-dose group and Low-dosage group than that in kindLing group (aLL P<0.05). ConcLusion? ASX couLd remarkabLy improve Learning and memory function of the epiLeptic rats. Antioxidative response and inhibition of apoptotic pathway were invoLved in this process.%目的 观察虾青素(ASX)对杏仁核电点燃癫痫大鼠模型学习记忆能力的改善作用,并检测海马氧化应激和凋亡指标以探讨其作用机制.方法 选取雄性成年SD大鼠,随机分为:对照组、癫痫组、高剂量ASX组(30mg·kg-1)、低剂量ASX组(15mg·kg-1)4组,每组15只.对照组仅给予电极植入,其余3组制备杏仁核慢性电点燃癫痫模型.ASX干预组分别于每天电刺激前1h给予ASX腹腔注射.在最后1次电刺激24h后行Morris水迷宫实验观察致痫大鼠学习记忆能力,检测各组大鼠海马组织中氧化应激参数的含量及凋亡参数蛋白表达水平.结果 ①Morris水迷宫实验:定位航行实验的1~5d,低剂量和高剂量ASX组的逃避潜伏期较癫痫组均明显缩短(均P<0.05),在空间探索实验中,低剂量和高剂量ASX组穿越平台次数较癫痫组均明显增多(均P<0.05);②海马氧化应激参数:低剂量和高剂量ASX组与癫痫组比较,丙二醛(MDA)含量均明显降低(均P<0.05),而谷胱甘肽(GSH)均明显升高(均P<0.05);③海马凋亡参数:低剂量和高剂量ASX组与癫痫组比较,BcL-2蛋白表达水平均明显升高(均P<0.05),而Bax蛋白表达水平均明显降低(均P<0.05).结论 ASX能够明显改善致痫大鼠的学习记忆能力,其机制与抗氧化及抗凋亡作用有关.