Sodium Butyrate Protects N2a Cells against Aβ Toxicity In Vitro. (15th April 2020)

• Record Type: Journal Article
• Authors: Sun, Jingxuan; Yuan, Boyu; Wu, Yancheng; Gong, Yuhong; Guo, Wenjin; Fu, Shoupeng; Luan, Yongxin; Wang, Wei
• Other Names: Dalmarco Eduardo Academic Editor.
• Is Part Of: Mediators of inflammation. Volume 2020(2020)
• Publication Date: 2020-04-15
• Subjects: Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1155/2020/7605160
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : Alzheimer's disease (AD) is a common neurodegenerative disease. A β 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 A β toxicity and to uncover the underlying mechanisms. The results showed that 2 mM NaB had a significant improvement effect on A β -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 A β -induced cell damage through activating GPR109A, which provides an innovative idea for the treatment of AD.