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• W2784743129 abstract "Previous studies have demonstrated that Vitexin possesses antihypertensive, anti-inflammatory and potential anticancer effects. The present study aimed to investigate whether the protective effect of vitexin protects against sevoflurane-induced neuronal apoptosis and the underlying mechanisms of this protective effect. The results demonstrated that Vitexin pretreatment significantly reduced neuronal apoptosis, and inhibited caspase-3 activity, apoptosis regulator BAX protein expression and malondialdehyde levels in sevoflurane-induced newborn rats. In addition, Vitexin pretreatment increased superoxide dismutase and glutathione peroxidase activity. Furthermore, it was revealed that treatment with vitexin induced hypoxia inducible factor 1α subunit (HIF-1α) and vascular endothelial growth factor (VEGF) protein expression, and suppressed phosphorylated-p38 MAP kinase (p38) protein expression in sevoflurane-induced newborn rat. Together, the results of the current study suggest that the protective effect of vitexin reduces sevoflurane-induced neuronal apoptosis through HIF-1α-, VEGF- and p38-associated signaling pathways in newborn rats." @default.
• W2784743129 created "2018-02-02" @default.
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• W2784743129 date "2018-01-17" @default.
• W2784743129 modified "2023-10-16" @default.
• W2784743129 title "Protective effect of vitexin reduces sevoflurane-induced neuronal apoptosis through HIF-1α, VEGF and p38 MAPK signaling pathway in�vitro and in newborn rats" @default.
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• W2784743129 doi "https://doi.org/10.3892/etm.2018.5758" @default.
• W2784743129 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5795406" @default.
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