Astaxanthin Inhibits H<sub>2</sub>O<sub>2</sub>-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR Activation
Oxidative stress, which damages cellular components and causes mitochondrial dysfunction, occurs in a variety of human diseases, including neurological disorders. The clearance of damaged mitochondria via mitophagy maintains the normal function of mitochondria and facilitates cell survival. Astaxant...
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MDPI AG
2024-01-01
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| Series: | Marine Drugs |
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| Online Access: | https://www.mdpi.com/1660-3397/22/2/57 |
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| author | Tingting Yan Feng Ding Yiting Zhang Yalin Wang Yinuo Wang Yuanqingzhi Zhang Feiyu Zhu Guanghan Zhang Xinyi Zheng Guangyin Jia Feng Zhou Yu Zhao Yan Zhao |
| author_facet | Tingting Yan Feng Ding Yiting Zhang Yalin Wang Yinuo Wang Yuanqingzhi Zhang Feiyu Zhu Guanghan Zhang Xinyi Zheng Guangyin Jia Feng Zhou Yu Zhao Yan Zhao |
| author_sort | Tingting Yan |
| collection | DOAJ |
| description | Oxidative stress, which damages cellular components and causes mitochondrial dysfunction, occurs in a variety of human diseases, including neurological disorders. The clearance of damaged mitochondria via mitophagy maintains the normal function of mitochondria and facilitates cell survival. Astaxanthin is an antioxidant known to have neuroprotective effects, but the underlying mechanisms remain unclear. This study demonstrated that astaxanthin inhibited H<sub>2</sub>O<sub>2</sub>-induced apoptosis in SH-SY5Y cells by ameliorating mitochondrial damage and enhancing cell survival. H<sub>2</sub>O<sub>2</sub> treatment significantly reduced the levels of activated Akt and mTOR and induced mitophagy, while pretreatment with astaxanthin prevented H<sub>2</sub>O<sub>2</sub>-induced inhibition of Akt and mTOR and attenuated H<sub>2</sub>O<sub>2</sub>-induced mitophagy. Moreover, the inhibition of Akt attenuated the protective effect of astaxanthin against H<sub>2</sub>O<sub>2</sub>-induced cytotoxicity. Taken together, astaxanthin might inhibit H<sub>2</sub>O<sub>2</sub>-induced apoptosis by protecting mitochondrial function and reducing mitophagy. The results also indicate that the Akt/mTOR signaling pathway was critical for the protection of astaxanthin against H<sub>2</sub>O<sub>2</sub>-induced cytotoxicity. The results from the present study suggest that astaxanthin can reduce neuronal oxidative injury and may have the potential to be used for preventing neurotoxicity associated with neurodegenerative diseases. |
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| language | English |
| last_indexed | 2024-03-07T22:24:20Z |
| publishDate | 2024-01-01 |
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| series | Marine Drugs |
| spelling | doaj.art-fe1147caddd6418c960432d4d3335ac22024-02-23T15:25:12ZengMDPI AGMarine Drugs1660-33972024-01-012225710.3390/md22020057Astaxanthin Inhibits H<sub>2</sub>O<sub>2</sub>-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR ActivationTingting Yan0Feng Ding1Yiting Zhang2Yalin Wang3Yinuo Wang4Yuanqingzhi Zhang5Feiyu Zhu6Guanghan Zhang7Xinyi Zheng8Guangyin Jia9Feng Zhou10Yu Zhao11Yan Zhao12Department of Bioengineering, Harbin Institute of Technology, Weihai 264209, ChinaDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, ChinaDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, ChinaDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, ChinaDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, ChinaDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, ChinaDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, ChinaDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, ChinaDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, ChinaDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, ChinaDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, ChinaDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, ChinaDepartment of Bioengineering, Harbin Institute of Technology, Weihai 264209, ChinaOxidative stress, which damages cellular components and causes mitochondrial dysfunction, occurs in a variety of human diseases, including neurological disorders. The clearance of damaged mitochondria via mitophagy maintains the normal function of mitochondria and facilitates cell survival. Astaxanthin is an antioxidant known to have neuroprotective effects, but the underlying mechanisms remain unclear. This study demonstrated that astaxanthin inhibited H<sub>2</sub>O<sub>2</sub>-induced apoptosis in SH-SY5Y cells by ameliorating mitochondrial damage and enhancing cell survival. H<sub>2</sub>O<sub>2</sub> treatment significantly reduced the levels of activated Akt and mTOR and induced mitophagy, while pretreatment with astaxanthin prevented H<sub>2</sub>O<sub>2</sub>-induced inhibition of Akt and mTOR and attenuated H<sub>2</sub>O<sub>2</sub>-induced mitophagy. Moreover, the inhibition of Akt attenuated the protective effect of astaxanthin against H<sub>2</sub>O<sub>2</sub>-induced cytotoxicity. Taken together, astaxanthin might inhibit H<sub>2</sub>O<sub>2</sub>-induced apoptosis by protecting mitochondrial function and reducing mitophagy. The results also indicate that the Akt/mTOR signaling pathway was critical for the protection of astaxanthin against H<sub>2</sub>O<sub>2</sub>-induced cytotoxicity. The results from the present study suggest that astaxanthin can reduce neuronal oxidative injury and may have the potential to be used for preventing neurotoxicity associated with neurodegenerative diseases.https://www.mdpi.com/1660-3397/22/2/57astaxanthinH<sub>2</sub>O<sub>2</sub>Akt/mTORapoptosismitophagy |
| spellingShingle | Tingting Yan Feng Ding Yiting Zhang Yalin Wang Yinuo Wang Yuanqingzhi Zhang Feiyu Zhu Guanghan Zhang Xinyi Zheng Guangyin Jia Feng Zhou Yu Zhao Yan Zhao Astaxanthin Inhibits H<sub>2</sub>O<sub>2</sub>-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR Activation Marine Drugs astaxanthin H<sub>2</sub>O<sub>2</sub> Akt/mTOR apoptosis mitophagy |
| title | Astaxanthin Inhibits H<sub>2</sub>O<sub>2</sub>-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR Activation |
| title_full | Astaxanthin Inhibits H<sub>2</sub>O<sub>2</sub>-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR Activation |
| title_fullStr | Astaxanthin Inhibits H<sub>2</sub>O<sub>2</sub>-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR Activation |
| title_full_unstemmed | Astaxanthin Inhibits H<sub>2</sub>O<sub>2</sub>-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR Activation |
| title_short | Astaxanthin Inhibits H<sub>2</sub>O<sub>2</sub>-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR Activation |
| title_sort | astaxanthin inhibits h sub 2 sub o sub 2 sub induced excessive mitophagy and apoptosis in sh sy5y cells by regulation of akt mtor activation |
| topic | astaxanthin H<sub>2</sub>O<sub>2</sub> Akt/mTOR apoptosis mitophagy |
| url | https://www.mdpi.com/1660-3397/22/2/57 |
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