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芝麻素通过激活Nrf2-ARE信号通路预防帕金森病。

Sesaminol prevents Parkinson's disease by activating the Nrf2-ARE signaling pathway.

作者信息

Kaji Haruka, Matsui-Yuasa Isao, Matsumoto Kayo, Omura Ayano, Kiyomoto Kunio, Kojima-Yuasa Akiko

机构信息

Department of Food and Human Health Sciences, Graduate School of Human Life Science, Osaka City University, 3-3-138 Sugimoto, Sumiyoshi-ku, Osaka, 558-8585, Japan.

Kiyomoto Co., Ltd., 6-1633 Totoro-cho, Nobeoka, Miyazaki, 889-0595, Japan.

出版信息

Heliyon. 2020 Nov 2;6(11):e05342. doi: 10.1016/j.heliyon.2020.e05342. eCollection 2020 Nov.

DOI:10.1016/j.heliyon.2020.e05342
PMID:33163674
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7609457/
Abstract

Parkinson's disease (PD) is a neurodegenerative disease caused by the degeneration of substantia nigra neurons due to oxidative stress. Sesaminol has strong antioxidant and anti-cancer effects. We investigated the preventive effect on PD as a new physiological action of sesaminol produced from sesaminol glycoside using and PD models. To prepare an PD model, 6-hydroxydopamine (6-OHDA) was added to human neuroblastoma (SH-SY5Y cells). The viability of SH-SY5Y cells decreased dose-dependently following 6-OHDA treatment, but the addition of sesaminol restored viability to the control level. 6-OHDA increased intracellular reactive oxygen species production, and the addition of sesaminol significantly suppressed this increase. No Nrf2 expression in the nucleus was observed in the control group, but a slight increase was observed in the 6-OHDA group. The sesaminol group showed strong expression of Nrf2 in the cytoplasm and nucleus. NAD(P)H: quinone oxidoreductase (NQO1) activity was enhanced in the 6-OHDA group and further enhanced in the sesaminol group. Furthermore, the neurotoxine rotenone was orally administrated to mice to prepare an PD model. The motor function of rotenone-treated mice was shorter than that of the control group, but a small amount of sesaminol restored it to the control level. The intestinal motility in the rotenone group was significantly lower than that in the control group, but it remained at the control level in the sesaminol group. The expression of α-synuclein in the substantia nigra increased in the rotenone group but decreased in the sesaminol group. The rotenone group exhibited shortening and damage to the colonic mucosa, but these abnormalities of the colonic mucosa were scarcely observed in the sesaminol group. These results suggest that sesaminol has a preventative effect on PD.

摘要

帕金森病（PD）是一种由于氧化应激导致黑质神经元变性而引起的神经退行性疾病。芝麻素酚具有强大的抗氧化和抗癌作用。我们使用[具体模型名称1]和[具体模型名称2]帕金森病模型，研究了芝麻素酚糖苷产生的芝麻素酚作为一种新的生理作用对帕金森病的预防效果。为制备[具体模型名称1]帕金森病模型，将6-羟基多巴胺（6-OHDA）添加到人神经母细胞瘤（SH-SY5Y细胞）中。6-OHDA处理后，SH-SY5Y细胞的活力呈剂量依赖性下降，但添加芝麻素酚可将活力恢复至对照水平。6-OHDA增加了细胞内活性氧的产生，而添加芝麻素酚可显著抑制这种增加。对照组未观察到细胞核中Nrf2的表达，但在6-OHDA组中观察到轻微增加。芝麻素酚组在细胞质和细胞核中均显示出Nrf2的强表达。NAD(P)H：醌氧化还原酶（NQO1）活性在6-OHDA组中增强，在芝麻素酚组中进一步增强。此外，将神经毒素鱼藤酮口服给予小鼠以制备[具体模型名称2]帕金森病模型。鱼藤酮处理的小鼠的运动功能比对照组短，但少量芝麻素酚可将其恢复至对照水平。鱼藤酮组的肠道蠕动明显低于对照组，但在芝麻素酚组中保持在对照水平。鱼藤酮组黑质中α-突触核蛋白的表达增加，但在芝麻素酚组中减少。鱼藤酮组表现出结肠黏膜缩短和损伤，但在芝麻素酚组中几乎未观察到结肠黏膜的这些异常。这些结果表明芝麻素酚对帕金森病具有预防作用。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/9b90248dda3b/sc1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/bdf15f309a42/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/8f18d77d35fa/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/5678c9168fb1/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/e78b4abf453e/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/650bcba402bf/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/ff61efba9a04/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/c7af3ed14b54/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/b9eb6a508066/gr11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/06413c52c09a/gr12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/cc53b4d29fff/gr13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/f0aa45d74669/gr14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/d4c5927e6546/gr15.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/ed8107214396/gr16.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/edb3c4807658/gr17.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc35/7609457/f57b1bfde324/sc2.jpg

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