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YY-1224，一种萜类三内酯强化的银杏叶提取物，通过抑制环氧化酶-2减轻由β-淀粉样蛋白（1-42）或APP和PS1双转基因过表达诱导的神经退行性变化。

YY-1224, a terpene trilactone-strengthened Ginkgo biloba, attenuates neurodegenerative changes induced by β-amyloid (1-42) or double transgenic overexpression of APP and PS1 via inhibition of cyclooxygenase-2.

作者信息

Li Zheng-Yi, Chung Yoon Hee, Shin Eun-Joo, Dang Duy-Khanh, Jeong Ji Hoon, Ko Sung Kwon, Nah Seung-Yeol, Baik Tae Gon, Jhoo Jin Hyeong, Ong Wei-Yi, Nabeshima Toshitaka, Kim Hyoung-Chun

机构信息

Neuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, Chunchon, 24341, Republic of Korea.

Department of Anatomy, College of Medicine, Chung-Ang University, Seoul, 06974, Republic of Korea.

出版信息

J Neuroinflammation. 2017 Apr 27;14(1):94. doi: 10.1186/s12974-017-0866-x.

DOI:10.1186/s12974-017-0866-x
PMID:28449688
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5408406/
Abstract

BACKGROUND

Ginkgo biloba has been reported to possess free radical-scavenging antioxidant activity and anti-inflammatory properties. In our pilot study, YY-1224, a terpene trilactone-strengthened extract of G. biloba, showed anti-inflammatory, neurotrophic, and antioxidant effects.

RESULTS

We investigated the pharmacological potential of YY-1224 in β-amyloid (Aβ) (1-42)-induced memory impairment using cyclooxygenase-2 (COX-2) knockout (-/-) and APPswe/PS1dE9 transgenic (APP/PS1 Tg) mice. Repeated treatment with YY-1224 significantly attenuated Aβ (1-42)-induced memory impairment in COX-2 (+/+) mice, but not in COX-2 (-/-) mice. YY-1224 significantly attenuated Aβ (1-42)-induced upregulation of platelet-activating factor (PAF) receptor gene expression, reactive oxygen species, and pro-inflammatory factors. In addition, YY-1224 significantly inhibited Aβ (1-42)-induced downregulation of PAF-acetylhydrolase-1 (PAF-AH-1) and peroxisome proliferator-activated receptor γ (PPARγ) gene expression. These changes were more pronounced in COX-2 (+/+) mice than in COX-2 (-/-) mice. YY-1224 significantly attenuated learning impairment, Aβ deposition, and pro-inflammatory microglial activation in APP/PS1 Tg mice, whereas it significantly enhanced PAF-AH and PPARγ expression. A preferential COX-2 inhibitor, meloxicam, did not affect the pharmacological activity by YY-1224, suggesting that the COX-2 gene is a critical mediator of the neuroprotective effects of YY-1224. The protective activity of YY-1224 appeared to be more efficacious than a standard G. biloba extract (Gb) against Aβ insult.

CONCLUSIONS

Our results suggest that the protective effects of YY-1224 against Aβ toxicity may be associated with its PAF antagonistic- and PPARγ agonistic-potential as well as inhibition of the Aβ-mediated pro-inflammatory switch of microglia phenotypes through suppression of COX-2 expression.

摘要

背景

据报道，银杏叶具有清除自由基的抗氧化活性和抗炎特性。在我们的初步研究中，YY - 1224，一种银杏叶的萜类三内酯强化提取物，显示出抗炎、神经营养和抗氧化作用。

结果

我们使用环氧合酶 - 2（COX - 2）基因敲除（-/-）和APPswe/PS1dE9转基因（APP/PS1 Tg）小鼠研究了YY - 1224对β - 淀粉样蛋白（Aβ）（1 - 42）诱导的记忆损伤的药理潜力。YY - 1224重复给药显著减轻了COX - 2（+/+）小鼠中Aβ（1 - 42）诱导的记忆损伤，但在COX - 2（-/-）小鼠中没有。YY - 1224显著减轻了Aβ（1 - 42）诱导的血小板活化因子（PAF）受体基因表达、活性氧和促炎因子的上调。此外，YY - 1224显著抑制了Aβ（1 - 42）诱导的PAF - 乙酰水解酶 - 1（PAF - AH - 1）和过氧化物酶体增殖物激活受体γ（PPARγ）基因表达的下调。这些变化在COX - 2（+/+）小鼠中比在COX - 2（-/-）小鼠中更明显。YY - 1224显著减轻了APP/PS1 Tg小鼠的学习损伤、Aβ沉积和促炎性小胶质细胞活化，而它显著增强了PAF - AH和PPARγ表达。一种选择性COX - 2抑制剂美洛昔康不影响YY - 1224的药理活性，表明COX - 2基因是YY - 1224神经保护作用的关键介质。YY - 1224的保护活性似乎比标准银杏叶提取物（Gb）对Aβ损伤更有效。

结论

我们的结果表明，YY - 1224对Aβ毒性的保护作用可能与其PAF拮抗和PPARγ激动潜力以及通过抑制COX - 2表达抑制Aβ介导的小胶质细胞表型促炎转换有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35aa/5408406/596bbcba2062/12974_2017_866_Fig13_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35aa/5408406/7e64563f9338/12974_2017_866_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35aa/5408406/5b84aae22a99/12974_2017_866_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35aa/5408406/82b6db12a05f/12974_2017_866_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35aa/5408406/a0f6a75955f6/12974_2017_866_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35aa/5408406/85c21f95967d/12974_2017_866_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35aa/5408406/4e7ee30702cc/12974_2017_866_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35aa/5408406/949214d992fa/12974_2017_866_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35aa/5408406/bcae26712c47/12974_2017_866_Fig12_HTML.jpg
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