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• W1926761645 endingPage "7704" @default.
• W1926761645 startingPage "7699" @default.
• W1926761645 abstract "Increasing evidence has indicated that the generation of reactive oxygen species (ROS) contributes to H2O2‑induced nerve injury. This may result in oxidative stress that leads to cell damage or death. Dietary or pharmaceutical augmentation of the endogenous antioxidant defense capacity is a potential means by which to prevent ROS‑induced damage. The aim of the current study was to investigate the effect of luteolin on H2O2‑induced cell apoptosis in cultured rat pheochromocytoma cells (PC12 cells) and to investigate the role of the phosphatidylinositol‑3‑kinase (PI3K)/protein kinase B (Akt) pathway on H2O2‑induced apoptosis. The results demonstrated that luteolin was able to inhibit the reduction in cell viability induced by H2O2. In addition, luteolin reduced ROS generation and lactate dehydrogenase release in H2O2‑treated PC12 cells. The levels of superoxide dismutase and glutathione peroxidase activity were increased following treatment with luteolin, however malondialdehyde levels were observed to be reduced. Additionally, luteolin increased the Bcl‑2/Bax ratio and enhanced Akt phosphorylation. However, these alterations were attenuated by pretreatment with an inhibitor of the PI3K/Akt pathway. In conclusion, luteolin inhibited H2O2‑induced apoptosis via reducing ROS levels and activating the PI3K/Akt pathway." @default.
• W1926761645 created "2016-06-24" @default.
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• W1926761645 creator A5085023720 @default.
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• W1926761645 date "2015-09-30" @default.
• W1926761645 modified "2023-10-16" @default.
• W1926761645 title "Luteolin-induced protection of H2O2-induced apoptosis in PC12 cells and the associated pathway" @default.
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• W1926761645 doi "https://doi.org/10.3892/mmr.2015.4400" @default.
• W1926761645 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26459830" @default.
• W1926761645 hasPublicationYear "2015" @default.
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