ReferenceID 3188
γ-mangostin attenuates amyloid-β42-induced neuroinflammation and oxidative stress in microglia-like BV2 cells via the mitogen-activated protein kinases signaling pathway
Eur J Pharmacol
Background: Oxidative stress (OS) and neuroinflammation are related to the pathogenic mechanism of Alzheimer's disease (AD). γ-Mangostin, a xanthone derivative obtained from mangosteen pericarp, could prevent their detri
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Record Fields
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- Reference Id
- 3188
- Evidence Id
- 19778
- Core Evidence Id
- 19778
- Source Reference Id
- 6356
- Herb2 Reference Id
- HBREF007153
- Subject Paper Key
- HBIN049149_34998794
- Pubmed Id
- 34998794
- Doi
- 10.1016/j.ejphar.2022.174744
- Paper Title
- γ-mangostin attenuates amyloid-β42-induced neuroinflammation and oxidative stress in microglia-like BV2 cells via the mitogen-activated protein kinases signaling pathway
- Paper Abstract
- Background: Oxidative stress (OS) and neuroinflammation are related to the pathogenic mechanism of Alzheimer's disease (AD). γ-Mangostin, a xanthone derivative obtained from mangosteen pericarp, could prevent their detrimental effects in AD. 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: Lactate dehydrogenase release assay and cell counting kit-8 assay were used to estimate the drug impact in BV2 cells and functional effects of the conditioned medium (supernatant of Aβ42 oligomers-/γ-mangostin-treated BV2 cells) on neuron-like SH-SY5Y and N2a cells. Quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay were carried out for detecting inflammatory factor contents. In addition, nitric oxide (NO) assay, an intracellular reactive oxygen species (ROS) assay, and qRT-PCR were performed to measure OS. Western blotting was used to explore the influence of γ-mangostin on the mitogen-activated protein kinase (MAPK) pathway. 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.
- Journal
- Eur J Pharmacol
- Publish Year
- 2022
- Experiment Subject
- Experiment Type
- Cell Experiment
- Phenotype Related
- Inflammation; Neuroinflammation; Alzheimer's Disease
- Paper Title Cn
- Paper Title En
- γ-mangostin attenuates amyloid-β42-induced neuroinflammation and oxidative stress in microglia-like BV2 cells via the mitogen-activated protein kinases signaling pathway
- Bilingual Status
- semi_complete