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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Antiamnesic Effect ofActinidia argutaExtract Intake in a Mouse Model of TMT-Induced Learning and Memory Dysfunction
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Antiamnesic Effect ofActinidia argutaExtract Intake in a Mouse Model of TMT-Induced Learning and Memory Dysfunction

机译:猕猴桃提取物摄入量对TMT诱导的学习和记忆功能障碍小鼠模型的记忆消除作用

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The antiamnesic effects of ethyl acetate fraction fromActinidia arguta(EFAA) on trimethyltin- (TMT-) induced memory impairment were investigated to find the possibility of functional food substances. EFAA showed a potent AChE inhibitory effect (IC50= 53 μg/mL) and efficient neuroprotection against H2O2-induced oxidative stress. The administration of EFAA significantly decreased TMT-induced cognitive deficit in Y-maze, passive avoidance, and Morris water maze (MWM) tests. After the behavioral tests, the antioxidant activities were confirmed using mice brain tissues. EFAA not only showed the inhibition of AChE activity and the decline of malondialdehyde (MDA) level as a sign of lipid peroxidation but also presented the increase of the superoxide dismutase (SOD) level and the decrease of the oxidized glutathione (GSSG)/total glutathione (GSH + GSSG) ratio. Finally, the phenolics in EFAA were identified using liquid chromatography coupled with hybrid triple quadrupole-linear ion trap mass spectrometry, and four main phenolics, such as quinic acid, chlorogenic acid, caffeoyl hexose, and quercetin-3-glucoside, were identified. These results suggest that EFAA containing physiological phenolics might enhance drug-induced amnesia through AChE inhibition and neuroprotection.
机译:研究了猕猴桃(EFAA)乙酸乙酯级分对三甲基锡(TMT-)引起的记忆障碍的抗记忆效应,以发现功能性食品物质的可能性。 EFAA具有有效的AChE抑制作用(IC50 =53μg/ mL),并且对H2O2引起的氧化应激具有有效的神经保护作用。 EFAA的使用在Y迷宫,被动回避和莫里斯水迷宫(MWM)测试中显着降低了TMT诱导的认知缺陷。行为测试后,使用小鼠脑组织确认了抗氧化活性。 EFAA不仅显示出对AChE活性的抑制和丙二醛(MDA)含量的下降,这是脂质过氧化的一个标志,而且还显示了超氧化物歧化酶(SOD)含量的增加和氧化型谷胱甘肽(GSSG)/总谷胱甘肽的下降(GSH + GSSG)比率。最后,通过液相色谱-混合三重四极杆-线性离子阱质谱法对EFAA中的酚进行了鉴定,并鉴定了四种主要酚,如奎尼酸,绿原酸,咖啡酰己糖和槲皮素-3-葡萄糖苷。这些结果表明,含有EFAA的生理酚类药物可能通过AChE抑制和神经保护作用增强药物诱发的健忘症。

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