Article Sidebar
Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Vitamin B2 blocks development of Alzheimer’s disease in APP/PS1 transgenic mice via anti-oxidative mechanism
Abstract
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
