Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylation
Trans-(-)-ε-viniferin (ε-viniferin) has antioxidative and anti-inflammatory effects. It also has neuroprotective effects in Huntington’s disease by activating the SIRT3/LKB1/AMPK signaling pathway; however, it remains unknown whether ε-viniferin also has a neuroprotective role in Parkinson’s disease...
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| Format: | Article |
| Language: | English |
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Wolters Kluwer Medknow Publications
2020-01-01
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| Series: | Neural Regeneration Research |
| Subjects: | |
| Online Access: | http://www.nrronline.org/article.asp?issn=1673-5374;year=2020;volume=15;issue=11;spage=2143;epage=2153;aulast=Zhang |
| _version_ | 1818139800870322176 |
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| author | Shuo Zhang Yan Ma Juan Feng |
| author_facet | Shuo Zhang Yan Ma Juan Feng |
| author_sort | Shuo Zhang |
| collection | DOAJ |
| description | Trans-(-)-ε-viniferin (ε-viniferin) has antioxidative and anti-inflammatory effects. It also has neuroprotective effects in Huntington’s disease by activating the SIRT3/LKB1/AMPK signaling pathway; however, it remains unknown whether ε-viniferin also has a neuroprotective role in Parkinson’s disease. A Parkinson’s disease cell model was induced by exposing SH-SY5Y cells to 3.0 μM rotenone for 24 hours, and cells were then treated with 1.0 μM ε-viniferin for 24 hours. Treatment with ε-viniferin upregulated SIRT3 expression, which promoted FOXO3 deacetylation and nuclear localization. ε-Viniferin also increased ATP production and decreased reactive oxygen species production. Furthermore, ε-viniferin treatment alleviated rotenone-induced mitochondrial depolarization and reduced cell apoptosis, and restored the expression of mitochondrial homeostasis-related proteins. However, when cells were transfected with SIRT3 or FOXO3 shRNA prior to rotenone and ε-viniferin treatment, these changes were reversed. The results from the present study indicate that ε-viniferin enhances SIRT3-mediated FOXO3 deacetylation, reduces oxidative stress, and maintains mitochondrial homeostasis, thus inhibiting rotenone-induced cell apoptosis. ε-Viniferin may therefore be a promising treatment strategy for Parkinson’s disease. |
| first_indexed | 2024-12-11T10:33:51Z |
| format | Article |
| id | doaj.art-555c8719efca42c4ae28e8aab2a2039f |
| institution | Directory Open Access Journal |
| issn | 1673-5374 |
| language | English |
| last_indexed | 2024-12-11T10:33:51Z |
| publishDate | 2020-01-01 |
| publisher | Wolters Kluwer Medknow Publications |
| record_format | Article |
| series | Neural Regeneration Research |
| spelling | doaj.art-555c8719efca42c4ae28e8aab2a2039f2022-12-22T01:10:48ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53742020-01-0115112143215310.4103/1673-5374.282264Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylationShuo ZhangYan MaJuan FengTrans-(-)-ε-viniferin (ε-viniferin) has antioxidative and anti-inflammatory effects. It also has neuroprotective effects in Huntington’s disease by activating the SIRT3/LKB1/AMPK signaling pathway; however, it remains unknown whether ε-viniferin also has a neuroprotective role in Parkinson’s disease. A Parkinson’s disease cell model was induced by exposing SH-SY5Y cells to 3.0 μM rotenone for 24 hours, and cells were then treated with 1.0 μM ε-viniferin for 24 hours. Treatment with ε-viniferin upregulated SIRT3 expression, which promoted FOXO3 deacetylation and nuclear localization. ε-Viniferin also increased ATP production and decreased reactive oxygen species production. Furthermore, ε-viniferin treatment alleviated rotenone-induced mitochondrial depolarization and reduced cell apoptosis, and restored the expression of mitochondrial homeostasis-related proteins. However, when cells were transfected with SIRT3 or FOXO3 shRNA prior to rotenone and ε-viniferin treatment, these changes were reversed. The results from the present study indicate that ε-viniferin enhances SIRT3-mediated FOXO3 deacetylation, reduces oxidative stress, and maintains mitochondrial homeostasis, thus inhibiting rotenone-induced cell apoptosis. ε-Viniferin may therefore be a promising treatment strategy for Parkinson’s disease.http://www.nrronline.org/article.asp?issn=1673-5374;year=2020;volume=15;issue=11;spage=2143;epage=2153;aulast=Zhangdeacetylation; foxo3; mitochondrial homeostasis; mitophagy; oxidative stress; parkinson’s disease; sirt3; ε-viniferin |
| spellingShingle | Shuo Zhang Yan Ma Juan Feng Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylation Neural Regeneration Research deacetylation; foxo3; mitochondrial homeostasis; mitophagy; oxidative stress; parkinson’s disease; sirt3; ε-viniferin |
| title | Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylation |
| title_full | Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylation |
| title_fullStr | Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylation |
| title_full_unstemmed | Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylation |
| title_short | Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylation |
| title_sort | neuroprotective mechanisms of ε viniferin in a rotenone induced cell model of parkinson s disease significance of sirt3 mediated foxo3 deacetylation |
| topic | deacetylation; foxo3; mitochondrial homeostasis; mitophagy; oxidative stress; parkinson’s disease; sirt3; ε-viniferin |
| url | http://www.nrronline.org/article.asp?issn=1673-5374;year=2020;volume=15;issue=11;spage=2143;epage=2153;aulast=Zhang |
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