Sodium butyrate exerts antioxidant stress effects and attenuates Aβ25-35-induced cytotoxicity in PC12 cells

Authors：Yuan, Boyu; Liu, Mingming; Gong, Yuhong; Wang, Zifan; Jin, Xinxin; Xie, Gaijie; Zhu, Mingqiang; Zhang, Xue; Luo, Siyuan; Qu, Qing; Zhu, Yufeng; Wang, Meng; Jin, Yingli^*; Li, Bai^*; Wang, Wei^*

Source：Archives of Biochemistry and Biophysics, 2022, 731: 109448.

DOI：10.1016/j.abb.2022.109448

• ANGIOTENSIN-CONVERTING ENZYME
• ALZHEIMERS-DISEASE
• MOUSE MODEL
• MECHANISMS
• RECEPTOR
• GPR109A
• PROTEIN
• NEUROTOXICITY
• ACTIVATION
• TOXICITY

Alzheimer's disease (AD), a common neurodegenerative disease, is characterised by the deposition of amyloid-beta (A beta) plaques and neurofibrillary tangles. An increasing number of studies have demonstrated that A beta causes neuronal damage and mitochondrial dysfunction. Herein, we evaluated the neuroprotective effect of sodium butyrate (NaB) against A beta induced neurotoxicity in PC12 cells. The results revealed that 3 mM of NaB promoted the expression of angiotensin-converting enzyme and brain-derived neurotrophic factor, which exert a neuroprotective effect by activating G protein-coupled receptors. Moreover, NaB could significantly improve mitochondrial dysfunction caused by A beta. In conclusion, NaB protected PC12 cells from A beta-induced cell damage, highlighting the potential of NaB in AD treatment.

• Institution
  吉林大学; 1; 仲恺农业工程学院; 南方医科大学