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作 者:邵盈盈[1,2] 李向荣[1] 李杰[1] 陈鑫[1] 袁丹[1]
机构地区:[1]浙江大学城市学院,浙江杭州310058310015 [2]浙江大学药学院,浙江杭州310058
出 处:《中国医院药学杂志》2013年第16期1330-1333,共4页Chinese Journal of Hospital Pharmacy
摘 要:目的:探讨紫心甘薯总黄酮(PSPF)对D-半乳糖致衰老小鼠学习记忆能力的影响及对小鼠脑组织氧化损伤的保护作用。方法:ICR小鼠随机分为6组(n=10):正常组(NC),模型组,维生素C组(100 mg.kg-1.d-1),PSPF低、中、高(50,100,200 mg.kg-1.d-1)剂量组。除正常组外,小鼠颈背部皮下注射D-半乳糖1 g.kg-1.d-1连续42 d,建立亚急性衰老模型,从造模第2周开始分别灌胃给予各组相应药物。42 d后采用Morris水迷宫法测定衰老小鼠学习记忆能力,同时测定小鼠脑组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-PX)活性。结果:与模型组相比,PSPF中、高剂量组能明显改善小鼠的衰老体征,缩短逃避潜伏期和空间搜索实验中第一次到达平台所在区域的时间(P<0.05),增加穿越平台所在区域的次数(P<0.05,P<0.01),并能有效提高衰老小鼠脑组织SOD和GSH-PX活性,降低MDA含量(P<0.05,P<0.01),呈现量效依赖关系。结论:PSPF能改善D-半乳糖致衰老小鼠的学习记忆能力,具有延缓衰老的作用,其作用机制可能与机体抗氧化酶活性增加,清除自由基、抗氧化能力提高所致。OBJECTIVE To investigate the effects of purple sweet potato flavonoids on learning ability and memory in senes- cent mice induced by D-galaetose and study the protective effect on oxidative injury in the brains of aging mice. METHODS ICR mice were randomly divided into 6 groups (n = 10) : normaI control group(NC), model group, vitamin C group (100 mgo kg- 1 . d-1 ) and PSPF groups (50, 100, 200 mg. kg -1. d- 1 ) ; except NC group, all the other groups were subcutaneously injec- ted with 1 g.kg-1 . d-1 D-galactose for successive 42 days to establish the sub-acute senescent model. All groups were given corresponding drugs respectively by intragastric administration 1 week later. Then the learning and memory ability of mice were measured by Morris water maze test, the amount of MDA in mouse brain tissue and the activities of SOD and GSH-PX were detected. RESULTS Compared with the model group, PSPF (100, 200 mg.kg-1.d-1 ) could significantly improve aging sign, reduce latent period to find the hidden platform and the time of first crossing the non-exits (P〈0. 05) and increase the number of crossing non-exits (P〈0. 05). PSPF could also effectively improve the activities of SOD and GSH-PX, reduce the amount of MDA (P〈0. 05, P〈0. 01 )with dose-dependent tendency. CONCLUSION PSPF can significantly improve the learning and memory ability of senescent mice induced by D-galactose, has the function of delaying senility. The mechanism may be related to its enhancement of activity of antioxidases, scavenging free radicals and improving the antioxidant ability.
分 类 号:R963[医药卫生—微生物与生化药学]
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