Version 1
: Received: 18 May 2017 / Approved: 19 May 2017 / Online: 19 May 2017 (06:26:45 CEST)
How to cite:
Wu, X.; Li, X.; Liang, S.; Liu, Y.; Dai, X.; Zheng, Q.; Sun, Y. Neuroprotective Effect of Anthocyanin Extract from Lycium ruthenicum Murray in Aβ1–42-induced Rat Model of AD. Preprints2017, 2017050144. https://doi.org/10.20944/preprints201705.0144.v1
Wu, X.; Li, X.; Liang, S.; Liu, Y.; Dai, X.; Zheng, Q.; Sun, Y. Neuroprotective Effect of Anthocyanin Extract from Lycium ruthenicum Murray in Aβ1–42-induced Rat Model of AD. Preprints 2017, 2017050144. https://doi.org/10.20944/preprints201705.0144.v1
Wu, X.; Li, X.; Liang, S.; Liu, Y.; Dai, X.; Zheng, Q.; Sun, Y. Neuroprotective Effect of Anthocyanin Extract from Lycium ruthenicum Murray in Aβ1–42-induced Rat Model of AD. Preprints2017, 2017050144. https://doi.org/10.20944/preprints201705.0144.v1
APA Style
Wu, X., Li, X., Liang, S., Liu, Y., Dai, X., Zheng, Q., & Sun, Y. (2017). Neuroprotective Effect of Anthocyanin Extract from <em>Lycium ruthenicum</em> Murray in Aβ1–42-induced Rat Model of AD. Preprints. https://doi.org/10.20944/preprints201705.0144.v1
Chicago/Turabian Style
Wu, X., Qiusheng Zheng and Yaxuan Sun. 2017 "Neuroprotective Effect of Anthocyanin Extract from <em>Lycium ruthenicum</em> Murray in Aβ1–42-induced Rat Model of AD" Preprints. https://doi.org/10.20944/preprints201705.0144.v1
Abstract
Alzheimer’s disease (AD) is an age-related neurodegenerative disease and is clinically characterized by cognitive impairment, memory loss, and personality disorder. Oligomers of amyloid beta-peptides (Aβ) and enhanced oxidative stress in senile plaques are prevalent pathologic hallmarks of AD. In this study, we detected the behavioral performance of Lycium ruthenicum Murray anthocyanin (LRA) -treated rats using the Morris water maze test and then investigated the effect of LRA on oxidative damage, neuronal apoptosis, and inflammatory response induced by Aβ1–42. Our results showed that LRA treatment markedly ameliorated the behavioral performance of Aβ1–42-induced rats and reduced the level of malondialdehyde, formation of protein carbonyl, and 8-hydroxy-2’-deoxygua-nosine. Furthermore, LRA also inhibited activated astrocytes and neuroinflammation via suppression of glial fibrillary acidic protein and tumor necrosis factor-alpha in the hippocampus of Aβ1–42-treated rat brain. These data suggest that LRA could be a potential anti-oxidant and anti-neuroinflammatory agent for the treatment of AD.
Biology and Life Sciences, Animal Science, Veterinary Science and Zoology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
