Vitamin B2 blocks development of Alzheimer’s disease in APP/PS1 transgenic mice via anti-oxidative mechanism
Purpose: To study the effect of vitamin B2 (VB2) on the development of Alzheimer’s disease (AD).
Methods: Memory and learning abilities were assessed in amyloid precursor protein/presenilin-1 (APP/PSI) transgenic mice aged 3 months, and C57BL/6 mice, using Morris water maze test. Brain tissue levels of key antioxidant enzymes, malondialdehyde (MDA), and reactive oxygen species (ROS) were assayed using ELISA kits. Western blot assay was used to monitor the expressions of Nrf2 and Keap1 proteins.
Results: Treatment with VB 2 significantly improved cognitive function of APP/PS1 mice with respect to number of crossings, duration of stay in target quadrant (TQ), and escape latency time (p < 0.01). Moreover, VB2 also significantly reduced the levels of MDA and ROS. It also brought about significant increases in brain activities of CAT, SOD, and GSH-Px in APP/PS1 mice, relative to the control group (p < 0.01). Moreover, VB2 up-regulated Nrf2 expression but down-regulated the expression of Keap1 in brain tissue of transgenic mice.
Conclusion: These results indicate that VB2 protects the brain from ROS-induced AD damage, most likely due to its potential anti-oxidant property and activation of the Nrf2 pathway.
Keywords: Alzheimer’s disease, Cognitive function, Vitamin B2, Reactive oxygen species, Superoxide oxide dismutase, Anti-oxidation