Quercetin Increases Mitochondrial Biogenesis and Reduces Free Radicals in Neuronal SH-SY5Y Cells
Alzheimer’s disease (AD) is a common neurodegenerative disorder that causes dementia and affects millions of people worldwide. The mechanism underlying AD is unclear; however, oxidative stress and mitochondrial biogenesis have been reported to be involved in AD progression. Previous research has als...
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MDPI AG
2022-08-01
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| Series: | Nutrients |
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| Online Access: | https://www.mdpi.com/2072-6643/14/16/3310 |
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| author | Chia-Ling Ho Ning-Jo Kao Ching-I Lin Tzu-Wen L. Cross Shyh-Hsiang Lin |
| author_facet | Chia-Ling Ho Ning-Jo Kao Ching-I Lin Tzu-Wen L. Cross Shyh-Hsiang Lin |
| author_sort | Chia-Ling Ho |
| collection | DOAJ |
| description | Alzheimer’s disease (AD) is a common neurodegenerative disorder that causes dementia and affects millions of people worldwide. The mechanism underlying AD is unclear; however, oxidative stress and mitochondrial biogenesis have been reported to be involved in AD progression. Previous research has also reported the reduction in mitochondrial biogenesis in the brains of patients with AD. Quercetin (QE), a type of polyphenol, has been found to be capable of increasing mitochondrial biogenesis in the body. Accordingly, we explored whether QE could reduce amyloid beta (Aβ) accumulation caused by hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced oxidative stress in SH-SY5Y cells. Our results revealed that QE stimulated the expression of mitochondrial-related proteins such as SIRT1, PGC-1α, and TFAM and subsequently activated mitochondrial biogenesis. Additionally, QE increased ADAM10 expression but reduced H<sub>2</sub>O<sub>2</sub>-induced reactive oxygen species production, apoptosis, β-site amyloid precursor protein cleaving enzyme 1 expression, and Aβ accumulation in the SH-SY5Y cells. These findings indicate that QE can effectively elevate mitochondrial biogenesis-related proteins and reduce the damage caused by oxidative stress, making it a promising option for protecting neuronal cells. |
| first_indexed | 2024-03-09T04:00:24Z |
| format | Article |
| id | doaj.art-631ef73c89594bbaa11262c2551ca863 |
| institution | Directory Open Access Journal |
| issn | 2072-6643 |
| language | English |
| last_indexed | 2024-03-09T04:00:24Z |
| publishDate | 2022-08-01 |
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| record_format | Article |
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| spelling | doaj.art-631ef73c89594bbaa11262c2551ca8632023-12-03T14:14:09ZengMDPI AGNutrients2072-66432022-08-011416331010.3390/nu14163310Quercetin Increases Mitochondrial Biogenesis and Reduces Free Radicals in Neuronal SH-SY5Y CellsChia-Ling Ho0Ning-Jo Kao1Ching-I Lin2Tzu-Wen L. Cross3Shyh-Hsiang Lin4School of Nutrition and Health Sciences, Taipei Medical University, Taipei 110, TaiwanDepartment of Nutrition and Health Sciences, Kainan University, Taoyuan 338, TaiwanDepartment of Nutrition and Health Sciences, Kainan University, Taoyuan 338, TaiwanDepartment of Nutrition Science, Purdue University, West Lafayette, IN 47907, USASchool of Nutrition and Health Sciences, Taipei Medical University, Taipei 110, TaiwanAlzheimer’s disease (AD) is a common neurodegenerative disorder that causes dementia and affects millions of people worldwide. The mechanism underlying AD is unclear; however, oxidative stress and mitochondrial biogenesis have been reported to be involved in AD progression. Previous research has also reported the reduction in mitochondrial biogenesis in the brains of patients with AD. Quercetin (QE), a type of polyphenol, has been found to be capable of increasing mitochondrial biogenesis in the body. Accordingly, we explored whether QE could reduce amyloid beta (Aβ) accumulation caused by hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced oxidative stress in SH-SY5Y cells. Our results revealed that QE stimulated the expression of mitochondrial-related proteins such as SIRT1, PGC-1α, and TFAM and subsequently activated mitochondrial biogenesis. Additionally, QE increased ADAM10 expression but reduced H<sub>2</sub>O<sub>2</sub>-induced reactive oxygen species production, apoptosis, β-site amyloid precursor protein cleaving enzyme 1 expression, and Aβ accumulation in the SH-SY5Y cells. These findings indicate that QE can effectively elevate mitochondrial biogenesis-related proteins and reduce the damage caused by oxidative stress, making it a promising option for protecting neuronal cells.https://www.mdpi.com/2072-6643/14/16/3310Aβoxidative stressquercetinmitochondrial biogenesisneurodegenerative disease |
| spellingShingle | Chia-Ling Ho Ning-Jo Kao Ching-I Lin Tzu-Wen L. Cross Shyh-Hsiang Lin Quercetin Increases Mitochondrial Biogenesis and Reduces Free Radicals in Neuronal SH-SY5Y Cells Nutrients Aβ oxidative stress quercetin mitochondrial biogenesis neurodegenerative disease |
| title | Quercetin Increases Mitochondrial Biogenesis and Reduces Free Radicals in Neuronal SH-SY5Y Cells |
| title_full | Quercetin Increases Mitochondrial Biogenesis and Reduces Free Radicals in Neuronal SH-SY5Y Cells |
| title_fullStr | Quercetin Increases Mitochondrial Biogenesis and Reduces Free Radicals in Neuronal SH-SY5Y Cells |
| title_full_unstemmed | Quercetin Increases Mitochondrial Biogenesis and Reduces Free Radicals in Neuronal SH-SY5Y Cells |
| title_short | Quercetin Increases Mitochondrial Biogenesis and Reduces Free Radicals in Neuronal SH-SY5Y Cells |
| title_sort | quercetin increases mitochondrial biogenesis and reduces free radicals in neuronal sh sy5y cells |
| topic | Aβ oxidative stress quercetin mitochondrial biogenesis neurodegenerative disease |
| url | https://www.mdpi.com/2072-6643/14/16/3310 |
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