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• W2978967636 abstract "Oxidative stress acts as an essential culprit factor in the development of stroke and Alzheimer’s disease. Norcepharadione B possesses various pharmacologic features as an extract obtained from Houttuynia cordata. Nevertheless, the anti-apoptotic and neuroprotective characteristics of norcepharadione B remain unclear. In this study, the neuronal protection effect provided by norcepharadione B against injury caused by hydrogen peroxide (H 2 O 2 ) in HT22 cell as well as the fundamental mechanism was systematically explored. The neurotoxicity assays of hippocampal cells, which were co-cultured with H 2 O 2 , showed that norcepharadione B had the ability to insulate the toxicity induced by H 2 O 2 with significant reduced cell apoptosis. Besides, norcepharadione B potentiated the activity of superoxide dismutase (SOD), increased the level of glutathione (GSH), and decreased malondialdehyde content. The H 2 O 2 -induced apoptotic protein Bax was suppressed, and the anti-apoptotic protein Bcl-2 was boosted by norcepharadione B. Norcepharadione B promoted Akt phosphorylation and further upregulated heme oxygenase (HO-1) in cells exposed to oxidative stress. However, the inductive effect of HO-1 by norcepharadione B was shut off via the PI3K/Akt inhibitor LY294002. Furthermore, 2-h incubation with H 2 O 2 substantially increased cell volume in HT22 cells, while norcepharadione B effectively alleviated such effect by interrupting the activation of VSOR Cl − channel. Collectively, our data revealed protective properties of norcepharadione B in resisting oxidative stress induced by H 2 O 2 through elevation of HO-1 in the dependence of PI3K/Akt and in inhibiting H 2 O 2 -induced cell swelling by VSOR Cl − channel obstruction in HT22 cells. Impact statement Norcepharadione B is an aporphine alkaloid compound extracted from Chinese herb Houttuynia cordata. It was well known for its anti-inflammatory, anti-cancer, and anti-platelet aggregation outcomes. Our study demonstrated that Norcepharadione B protected hippocampal neurons against oxidative stress and the resultant cell apoptosis upon H 2 O 2 exposure. Meanwhile, Norcepharadione B also substantially reduced cell swelling induced by H 2 O 2 via inhibiting VSOR Cl − channel in neurons. These findings uncovered the potential mechanisms of Norcepharadione B in protecting neuron apoptosis under oxidative stress and propose that Norcepharadione B may serve as a favorable herb medicine for restoring neuronal injury in the pathogenesis of stroke together with other neurodegenerative diseases." @default.
• W2978967636 created "2019-10-10" @default.
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• W2978967636 date "2019-10-04" @default.
• W2978967636 modified "2023-10-17" @default.
• W2978967636 title "Norcepharadione B attenuates H₂O₂-induced neuronal injury by upregulating cellular antioxidants and inhibiting volume-sensitive Cl⁻ channel" @default.
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• W2978967636 doi "https://doi.org/10.1177/1535370219881358" @default.
• W2978967636 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6900699" @default.
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