Abstract | BACKGROUND: OBJECTIVE: This study focused on determining the role of γ- mangostin in protection against the amyloid-β (Aβ) 42 oligomers-induced OS and inflammation in microglial BV2 cells and investigating their precise mechanism of action. METHODS: RESULTS: γ- Mangostin alleviated Aβ42 oligomer-induced inflammation by decreasing the levels of interleukin (IL) -6, IL-1β, and tumor necrosis factor-α, while attenuating OS through decreasing ROS/NO generation, and suppressing cyclo-oxygenase-2 and inducible NO synthase expressions. γ- Mangostin protected N2a and SH-SY5Ycells against the BV2 cell supernatant-induced toxicity following Aβ42 oligomer exposure. Furthermore, γ- mangostin inhibited c-Jun NH2-terminal kinase and p38 MAPK pathway activation. CONCLUSION: This study demonstrated that γ- mangostin could attenuate OS and inflammation resulting from Aβ42 oligomers, which also protect neurons against toxic medium-induced injury, suggesting that it may exert a protective effect in AD.
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Authors | Chaojun Kong, Longfei Jia, Jianping Jia |
Journal | European journal of pharmacology
(Eur J Pharmacol)
Vol. 917
Pg. 174744
(Feb 15 2022)
ISSN: 1879-0712 [Electronic] Netherlands |
PMID | 34998794
(Publication Type: Journal Article)
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Copyright | Copyright © 2022. Published by Elsevier B.V. |
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