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提取物通过下调淀粉样蛋白-β表达和上调脑源性神经营养因子/酪氨酸激酶受体B通路改善东莨菪碱处理小鼠的记忆。

Extract Improves Memory in Scopolamine-Treated Mice via Downregulating Amyloid-β Expression and Upregulating BDNF/TrkB Pathway.

作者信息

Baek Seung Yeon, Li Fu Yi, Kim Da Hee, Kim Su Jin, Kim Mee Ree

机构信息

Department of Food and Nutrition, Chungnam National University, Daejeon 34134, Korea.

出版信息

Antioxidants (Basel). 2020 Jul 15;9(7):620. doi: 10.3390/antiox9070620.

DOI:10.3390/antiox9070620
PMID:32679768
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7402154/
Abstract

, a green alga, has long been used in food diets as well as traditional remedies in East Asia. Our preliminary study demonstrated that an ethyl acetate extract of (EAEP) exhibited the strongest antioxidant activity compared to ethanol or water extracts. Nonetheless, there has been no report on the effect of EAEP on memory impairment due to oxidative damage. This study investigated whether EAEP could attenuate memory deficits in an oxidative stress-induced mouse model. EAEP was orally administered (50 or 100 mg/kg body weight (b.w.)) to mice and then scopolamine was administered. The oral administration of EAEP at 100 mg/kg b.w. significantly restored memory impairments induced by scopolamine, as evaluated by the Morris water maze test, and the passive avoidance test. Further, EAEP upregulated the protein expression of BDNF, p-CREB, p-TrkB, and p-Akt. Moreover, EAEP downregulated the expression of amyloid-β, tau, and APP. The regulation of cholinergic marker enzyme activities and the protection of neuronal cells from oxidative stress-induced cell death in the brain of mice via the downregulation of amyloid-β and the upregulation of the BDNF/TrkB pathway by EAEP suggest its potential as a pharmaceutical candidate to prevent neurodegenerative diseases.

摘要

绿藻长期以来一直被用于东亚的食品饮食以及传统疗法中。我们的初步研究表明,与乙醇或水提取物相比,绿藻的乙酸乙酯提取物(EAEP)表现出最强的抗氧化活性。尽管如此,尚未有关于EAEP对氧化损伤所致记忆障碍影响的报道。本研究调查了EAEP是否能减轻氧化应激诱导的小鼠模型中的记忆缺陷。将EAEP以50或100毫克/千克体重(b.w.)口服给予小鼠,然后给予东莨菪碱。通过莫里斯水迷宫试验和被动回避试验评估,以100毫克/千克b.w.口服EAEP可显著恢复东莨菪碱诱导的记忆损伤。此外,EAEP上调了BDNF、p-CREB、p-TrkB和p-Akt的蛋白表达。此外,EAEP下调了淀粉样蛋白-β、tau和APP的表达。EAEP通过下调淀粉样蛋白-β和上调BDNF/TrkB途径对小鼠大脑中胆碱能标记酶活性的调节以及对神经元细胞免受氧化应激诱导的细胞死亡的保护作用表明其作为预防神经退行性疾病的药物候选物的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78d8/7402154/763455b0ab16/antioxidants-09-00620-g008.jpg
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