UCP2 protects against amyloid beta toxicity and oxidative stress in primary neuronal culture

AD is a common neurodegenerative disease characterized by aggregated amyloid-beta (Aβ) peptide, and oxidative stress, while uncoupling protein 2 (UCP2) is a member of the anion carrier family, predicted the existence of a protein-regulated proton leak with the main purpose of controlling mitochondrial oxidative stress, reduce the generation of superoxide anion. we use the primary hippocampal neurons and add the different doses of Aβ1-40, then observe the change of UCP2 at different concentrations of Aβ, activity of LDH and the content of NO. Our results provide novel insight that UCP2 may protect hippocampal neurons exposed to amyloid β protein through decreasing ROS production. 20 μmol/L Aβ1-40 significantly increased the activity of LDH and the content of NO. According to the correlation analysis, NO was significantly correlation with LDH, and UCP2 was significantly correlation with NO. These results suggest the potential of UCP2 as a therapeutic candidate for treating neurodegenerative diseases such as AD.