银杏叶提取物对阿尔茨海默病模型大鼠神经功能的影响  

Effect of Ginkgo biloba extract on neurological function in Alzheimer's disease modal rats

作　　者：余研[1] 吴志峰[1] 秦毅辉[1] 李毅[1] Yu Yan Wu Zhifeng Qin Yihui Li Yi(Department of Cadre Ward, the 174th Hospital of PLA, Xiamen, Fujian 361003, China)

机构地区：[1]解放军174医院干部病房老年科,厦门361003

出　　处：《中国微侵袭神经外科杂志》2017年第6期275-278,共4页Chinese Journal of Minimally Invasive Neurosurgery

摘　　要：目的探讨银杏叶提取物(GBE)对阿尔茨海默病(AD)模型大鼠学习和记忆行为、海马组织中氧化自由基及内质网应激的影响。方法腹腔注射D-半乳糖诱导构建大鼠AD模型。将15个月龄的雄性Wistar大鼠,随机分为对照组、AD组、AD+GBE组、AD+GBE+内质网应激诱导剂衣霉素(AD+GBE+Tm组),每组12只。采用Morris水迷宫测定大鼠学习和记忆行为;试剂盒检测海马组织超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量;Western blot方法测定激活转录因子6(ATF-6)和CCAAT/增强子结合蛋白(CHOP)的表达。结果与对照组比较,AD组、AD+GBE组和AD+GBE+Tm组大鼠逃避潜伏期明显延长,目标象限内游泳距离占总距离的百分比明显降低,海马组织氧化自由基MDA、抗氧化酶SOD和内质网相关因子(ATF-6、CHOP)蛋白表达上调(P<0.05);与AD组比较,AD+GBE组大鼠逃避潜伏期明显缩短,目标象限内游泳距离占总距离的百分比明显增加(P<0.05),海马组织中氧化自由基MDA表达降低,抗氧化酶SOD活性增加;同时内质网应激相关因子ATF-6和CHOP蛋白表达减少(P<0.05)。与AD+GBE组比较,AD+GBE+Tm组氧化自由基MDA表达增加,抗氧化酶SOD活性降低;内质网应激相关因子ATF-6和CHOP蛋白表达增加(P<0.05)。结论 GBE能抑制内质网应激反应,抑制氧化自由基产生,改善AD模型大鼠学习和记忆功能,缓解AD病情。Objective To investigate the effects of Ginkgo biloba extract （GBE） on learning and memory behaviors, oxyradical of the hippocampus tissue and endoplasmic reticulum stress （ERS） response in Alzheimer＇s disease （AD） model rats. Methods AD model rats were established by intraperitoneal injection of D-galactose. The 15 months old Wistar rats were randomly and equally divided into 4 groups： control group, AD group, AD ＋ GBE group and ERS activator tunicamycin （Tm） group （AD ＋ GBE ＋ Tin group）. The learning and memory behaviors were examined by the Morris water maze. The superoxide dismutase （SOD） activity and malondialdehyde （MDA） content of the hippocampus tissue were detected by kit. Activating transcription factor 6 （ATF-6） and CCAAT/enhancer- binding protein homologous protein （CHOP） were tested with Western blotting. Results Compared with the control group, the escape latency was prolonged, while the distance percentage in target quadrant was decreased, and the expressions of MDA, SOX, ATF-6 and CHOP were up-regulated in the other three groups （P 〈 0.05）. Compared with the AD group, the escape latency was obviously shortened and the distance percentage in target quadrant was increased, meanwhile, SOD expression was up-regulated, and the expressions of MDA, ATF-6 and CHOP were down-regulated in the AD ＋ GBE group （P 〈 0.05）. Compared with the AD ＋ GBE group, SOD expression was down-regulated and the expressions of MDA, ATP-6 and CHOP were up-regulated （P 〈 0.05）. Conclusions GBE can inhibit ERS response and suppress the generation of oxyradicals, which can improve learning and memory behaviors of AD modal rats and relieve the disease condition.

关 键 词：阿尔茨海默病 银杏叶提取物 内质网应激 神经保护 大鼠 

分 类 号：R285.5[医药卫生—中药学] R-332[医药卫生—中医学]