Sodium Butyrate Protects N2a Cells against Aβ Toxicity In Vitro
Alzheimer’s disease (AD) is a common neurodegenerative disease. Aβ plays an important role in the pathogenesis of AD. Sodium butyrate (NaB) is a short-chain fatty acid salt that exerts neuroprotective effects such as anti-inflammatory, antioxidant, antiapoptotic, and cognitive improvement in central...
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| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2020-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2020/7605160 |
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| author | Jingxuan Sun Boyu Yuan Yancheng Wu Yuhong Gong Wenjin Guo Shoupeng Fu Yongxin Luan Wei Wang |
| author_facet | Jingxuan Sun Boyu Yuan Yancheng Wu Yuhong Gong Wenjin Guo Shoupeng Fu Yongxin Luan Wei Wang |
| author_sort | Jingxuan Sun |
| collection | DOAJ |
| description | Alzheimer’s disease (AD) is a common neurodegenerative disease. Aβ plays an important role in the pathogenesis of AD. Sodium butyrate (NaB) is a short-chain fatty acid salt that exerts neuroprotective effects such as anti-inflammatory, antioxidant, antiapoptotic, and cognitive improvement in central nervous system diseases. The aim of this study is to research the protective effects of NaB on neurons against Aβ toxicity and to uncover the underlying mechanisms. The results showed that 2 mM NaB had a significant improvement effect on Aβ-induced N2a cell injury, by increasing cell viability and reducing ROS to reduce injury. In addition, by acting on the GPR109A receptor, NaB regulates the expression of AD-related genes such as APP, NEP, and BDNF. Therefore, NaB protects N2a cells from Aβ-induced cell damage through activating GPR109A, which provides an innovative idea for the treatment of AD. |
| format | Article |
| id | doaj-art-2aca012e42af468bafd1e3acb2514c8d |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2020-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-2aca012e42af468bafd1e3acb2514c8d2025-02-03T05:44:15ZengWileyMediators of Inflammation0962-93511466-18612020-01-01202010.1155/2020/76051607605160Sodium Butyrate Protects N2a Cells against Aβ Toxicity In VitroJingxuan Sun0Boyu Yuan1Yancheng Wu2Yuhong Gong3Wenjin Guo4Shoupeng Fu5Yongxin Luan6Wei Wang7Key Laboratory of Zoonosis Research, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130062, ChinaKey Laboratory of Zoonosis Research, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130062, ChinaKey Laboratory of Zoonosis Research, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130062, ChinaKey Laboratory of Zoonosis Research, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130062, ChinaKey Laboratory of Zoonosis Research, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130062, ChinaKey Laboratory of Zoonosis Research, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130062, ChinaFirst Clinical Hospital of Jilin University, Changchun, ChinaKey Laboratory of Zoonosis Research, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun 130062, ChinaAlzheimer’s disease (AD) is a common neurodegenerative disease. Aβ plays an important role in the pathogenesis of AD. Sodium butyrate (NaB) is a short-chain fatty acid salt that exerts neuroprotective effects such as anti-inflammatory, antioxidant, antiapoptotic, and cognitive improvement in central nervous system diseases. The aim of this study is to research the protective effects of NaB on neurons against Aβ toxicity and to uncover the underlying mechanisms. The results showed that 2 mM NaB had a significant improvement effect on Aβ-induced N2a cell injury, by increasing cell viability and reducing ROS to reduce injury. In addition, by acting on the GPR109A receptor, NaB regulates the expression of AD-related genes such as APP, NEP, and BDNF. Therefore, NaB protects N2a cells from Aβ-induced cell damage through activating GPR109A, which provides an innovative idea for the treatment of AD.http://dx.doi.org/10.1155/2020/7605160 |
| spellingShingle | Jingxuan Sun Boyu Yuan Yancheng Wu Yuhong Gong Wenjin Guo Shoupeng Fu Yongxin Luan Wei Wang Sodium Butyrate Protects N2a Cells against Aβ Toxicity In Vitro Mediators of Inflammation |
| title | Sodium Butyrate Protects N2a Cells against Aβ Toxicity In Vitro |
| title_full | Sodium Butyrate Protects N2a Cells against Aβ Toxicity In Vitro |
| title_fullStr | Sodium Butyrate Protects N2a Cells against Aβ Toxicity In Vitro |
| title_full_unstemmed | Sodium Butyrate Protects N2a Cells against Aβ Toxicity In Vitro |
| title_short | Sodium Butyrate Protects N2a Cells against Aβ Toxicity In Vitro |
| title_sort | sodium butyrate protects n2a cells against aβ toxicity in vitro |
| url | http://dx.doi.org/10.1155/2020/7605160 |
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