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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/29730


    標題: Luteolin and Apigenin Attenuate 4-Hydroxy-2-Nonenal-Mediated Cell Death through Modulation of UPR, Nrf2-ARE and MAPK Pathways in PC12 Cells
    作者: Wu, Pei-Shan
    Yen, Jui-Hung
    Kou, Mei-Chun
    Wu, Ming-Jiuan
    貢獻者: 生物科技系
    關鍵字: Endoplasmic-reticulum stress
    Unfolded protein response
    Heme oxygenase-1 expression
    lipid-peroxidation product
    Glutamate cysteine ligase
    Factor-kappa-b
    Oxidative stress
    er stress
    cystine/glutamatea ntiporter
    transcription factor
    日期: 2015-06
    上傳時間: 2016-04-19 19:06:09 (UTC+8)
    出版者: Public Library Science
    摘要: Luteolin and apigenin are dietary flavones and exhibit a broad spectrum of biological activities including antioxidant, anti-inflammatory, anti-cancer and neuroprotective effects. The lipid peroxidation product 4-hydroxy-2-nonenal (4-HNE) has been implicated as a causative agent in the development of neurodegenerative disorders. This study investigates the cytoprotective effects of luteolin and apigenin against 4-HNE-mediated cytotoxicity in neuronal-like catecholaminergic PC12 cells. Both flavones restored cell viability and repressed caspase-3 and PARP-1 activation in 4-HNE-treated cells. Luteolin also mitigated 4-HNE-mediated LC3 conversion and reactive oxygen species (ROS) production. Luteolin and apigenin up-regulated 4-HNE-mediated unfolded protein response (UPR), leading to an increase in endoplasmic reticulum chaperone GRP78 and decrease in the expression of UPR-targeted pro-apoptotic genes. They also induced the expression of Nrf2-targeted HO-1 and xCT in the absence of 4-HNE, but counteracted their expression in the presence of 4-HNE. Moreover, we found that JNK and p38 MAPK inhibitors significantly antagonized the increase in cell viability induced by luteolin and apigenin. Consistently, enhanced phosphorylation of JNK and p38 MAPK was observed in luteolin-and apigenin-treated cells. In conclusion, this result shows that luteolin and apigenin activate MAPK and Nrf2 signaling, which elicit adaptive cellular stress response pathways, restore 4-HNE-induced ER homeostasis and inhibit cytotoxicity. Luteolin exerts a stronger cytoprotective effect than apigenin possibly due to its higher MAPK, Nrf2 and UPR activation, and ROS scavenging activity.
    關聯: Plos One, v.10 n.6, Article ID e0130599
    Appears in Collections:[生物科技系(所)] 期刊論文

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