English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Among a series of xanthones identified from mangosteen, the fruit of  Garcinia mangostana  L. (Guttifereae),  α - and  γ -mangostins are known to be major constituents exhibiting diverse biological activities. However, the effects of  γ -mangostin on oxidative neurotoxicity and impaired memory are yet to be elucidated. In the present study, the protective effect of  γ -mangostin on oxidative stress-induced neuronal cell death and its underlying action mechanism(s) were investigated and compared to that of  α -mangostin using primary cultured rat cortical cells. In addition, the effect of orally administered  γ -mangostin on scopolamine-induced memory impairment was evaluated in mice. We found that  γ -mangostin exhibited prominent protection against H 2 O 2 - or xanthine/xanthine oxidase-induced oxidative neuronal death and inhibited reactive oxygen species (ROS) generation triggered by these oxidative insults. In contrast,  α -mangostin had no effects on the oxidative neuronal damage or associated ROS production. We also found that  γ -mangostin, not  α -mangostin, significantly inhibited H 2 O 2 -induced DNA fragmentation and activation of caspases 3 and 9, demonstrating its antiapoptotic action. In addition, only  γ -mangostin was found to effectively inhibit lipid peroxidation and DPPH radical formation, while both mangostins inhibited  β -secretase activity. Furthermore, we observed that the oral administration of  γ -mangostin at dosages of 10 and 30 mg/kg markedly improved scopolamine-induced memory impairment in mice. Collectively, these results provide both  in vitro  and  in vivo  evidences for the neuroprotective and memory enhancing effects of  γ -mangostin. Multiple mechanisms underlying this neuroprotective action were suggested in this study. Based on our findings,  γ -mangostin could serve as a potentially preferable candidate over  α -mangostin in combatting oxidative stress-associated neurodegenerative diseases including Alzheimer's disease.

Inhibition of Oxidative Neurotoxicity and Scopolamine-Induced Memory Impairment by γ-Mangostin: In Vitro and In Vivo Evidence