Sodium Butyrate Protects N2a Cells against A<i>β</i> Toxicity In Vitro

Abstract

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