Sesaminol prevents Parkinson's disease by activating the Nrf2-ARE signaling pathway
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...
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| Format: | Article |
| Language: | English |
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Elsevier
2020-11-01
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| Series: | Heliyon |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S240584402032185X |
| _version_ | 1819176030966906880 |
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| author | Haruka Kaji Isao Matsui-Yuasa Kayo Matsumoto Ayano Omura Kunio Kiyomoto Akiko Kojima-Yuasa |
| author_facet | Haruka Kaji Isao Matsui-Yuasa Kayo Matsumoto Ayano Omura Kunio Kiyomoto Akiko Kojima-Yuasa |
| author_sort | Haruka Kaji |
| collection | DOAJ |
| description | 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 in vitro and in vivo PD models. To prepare an in vitro 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 in vivo 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. |
| first_indexed | 2024-12-22T21:04:17Z |
| format | Article |
| id | doaj.art-a8f5f5343c2142b482cc139660ca01d1 |
| institution | Directory Open Access Journal |
| issn | 2405-8440 |
| language | English |
| last_indexed | 2024-12-22T21:04:17Z |
| publishDate | 2020-11-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Heliyon |
| spelling | doaj.art-a8f5f5343c2142b482cc139660ca01d12022-12-21T18:12:44ZengElsevierHeliyon2405-84402020-11-01611e05342Sesaminol prevents Parkinson's disease by activating the Nrf2-ARE signaling pathwayHaruka Kaji0Isao Matsui-Yuasa1Kayo Matsumoto2Ayano Omura3Kunio Kiyomoto4Akiko Kojima-Yuasa5Department of Food and Human Health Sciences, Graduate School of Human Life Science, Osaka City University, 3-3-138 Sugimoto, Sumiyoshi-ku, Osaka, 558-8585, JapanDepartment of Food and Human Health Sciences, Graduate School of Human Life Science, Osaka City University, 3-3-138 Sugimoto, Sumiyoshi-ku, Osaka, 558-8585, JapanDepartment of Food and Human Health Sciences, Graduate School of Human Life Science, Osaka City University, 3-3-138 Sugimoto, Sumiyoshi-ku, Osaka, 558-8585, JapanKiyomoto Co., Ltd., 6-1633 Totoro-cho, Nobeoka, Miyazaki, 889-0595, JapanKiyomoto Co., Ltd., 6-1633 Totoro-cho, Nobeoka, Miyazaki, 889-0595, JapanDepartment 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; Corresponding author.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 in vitro and in vivo PD models. To prepare an in vitro 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 in vivo 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.http://www.sciencedirect.com/science/article/pii/S240584402032185XNeuroscienceNutritionNatural productOxidative stressAntioxidantSesaminol |
| spellingShingle | Haruka Kaji Isao Matsui-Yuasa Kayo Matsumoto Ayano Omura Kunio Kiyomoto Akiko Kojima-Yuasa Sesaminol prevents Parkinson's disease by activating the Nrf2-ARE signaling pathway Heliyon Neuroscience Nutrition Natural product Oxidative stress Antioxidant Sesaminol |
| title | Sesaminol prevents Parkinson's disease by activating the Nrf2-ARE signaling pathway |
| title_full | Sesaminol prevents Parkinson's disease by activating the Nrf2-ARE signaling pathway |
| title_fullStr | Sesaminol prevents Parkinson's disease by activating the Nrf2-ARE signaling pathway |
| title_full_unstemmed | Sesaminol prevents Parkinson's disease by activating the Nrf2-ARE signaling pathway |
| title_short | Sesaminol prevents Parkinson's disease by activating the Nrf2-ARE signaling pathway |
| title_sort | sesaminol prevents parkinson s disease by activating the nrf2 are signaling pathway |
| topic | Neuroscience Nutrition Natural product Oxidative stress Antioxidant Sesaminol |
| url | http://www.sciencedirect.com/science/article/pii/S240584402032185X |
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