| First Author | Lim J | Year | 2022 |
| Journal | Molecules | Volume | 27 |
| Issue | 24 | PubMed ID | 36557811 |
| Mgi Jnum | J:351344 | Mgi Id | MGI:7663172 |
| Doi | 10.3390/molecules27248678 | Citation | Lim J, et al. (2022) Verbenalin Reduces Amyloid-Beta Peptide Generation in Cellular and Animal Models of Alzheimer's Disease. Molecules 27(24) |
| abstractText | Verbenalin, among the major constituents of Verbena officinalis, has been reported to exhibit sleep-promoting and antioxidant activities. This study demonstrates the effects of verbenalin on amyloid-beta (Abeta) peptide generation in Swedish mutant amyloid precursor protein (APP)-overexpressing Neuro2a cells (SweAPP/N2a) and in Alzheimer's disease (AD) animal models. We further performed molecular biological analyses of these in vitro and in vivo models of AD. The effects of verbenalin were assessed based on the expression of factors related to Abeta peptide production using Western blotting, enzyme-linked immunosorbent assay, and immunohistochemistry (IHC). The intracellular expression and release of APP protein were both decreased by verbenalin treatment in SweAPP/N2a cells. Thus, the production of Abeta peptides was decreased. Compared to those in AD transgenic (Tg) mice, IHC revealed that verbenalin-treated animals showed decreased Abeta and tau expression levels in the hippocampus. In addition, verbenalin restored the expression of brain-derived neurotrophic factor (BDNF) in the hippocampus of AD animal models. These findings suggest that verbenalin may decrease Abeta formation both in vitro and in vivo. Verbenalin may also help improve the pathological hallmarks of AD. |
