Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/28617
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    標題: Luteolin Modulates 6-Hydroxydopamine-Induced Transcriptional Changes of Stress Response Pathways in PC12 Cells
    作者: Hu, Ling-Wei
    Yen, Jui-Hung
    Shen, Yi-Ting
    Wu, Kuan-Yi
    Wu, Ming-Jiuan
    貢獻者: 生物科技系
    藥學系
    關鍵字: ENDOPLASMIC-RETICULUM STRESS
    UNFOLDED PROTEIN RESPONSE
    HEME OXYGENASE-1 EXPRESSION
    NERVE GROWTH-FACTOR
    OXIDATIVE STRESS
    PARKINSONS-DISEASE
    ER STRESS
    DNA-DAMAGE
    LIPID-PEROXIDATION
    GENE-EXPRESSION
    日期: 2014-05
    上傳時間: 2015-05-06 21:22:40 (UTC+8)
    出版者: Public Library Science
    摘要: The neurotoxin 6-hydroxydopamine (6-OHDA), which causes transcriptional changes associated with oxidative and proteotoxic stress, has been widely used to generate an experimental model of Parkinson's disease. The food-derived compound luteolin has multi-target actions including antioxidant, anti-inflammatory and neurotrophic activities. The aim of this study is to investigate how luteolin affects 6-OHDA-mediated stress response pathways. The results showed that when PC12 cells were pre-treated with luteolin (20 mu M) 30 min prior to 6-OHDA (100 mu M) exposure, 6-OHDA-induced ROS overproduction, cytotoxicity, caspase-3 activation, and mRNA expression of BIM, TRB3 and GADD34 were significantly attenuated. Moreover, 6-OHDA-mediated cell cycle arrest and transcription of p53 target genes, p21, GADD45 alpha and PUMA, were reduced by luteolin. Luteolin also significantly down-regulated 6-OHDA-mediated unfolded protein response (UPR), leading to decreases in phospho-eIF2 alpha, ATF4, GRP78 and CHOP. In addition, luteolin attenuated 6-OHDA-induced Nrf2-mediated HO-1 and GCLC. Taken together, these results suggest that diminishing intracellular ROS formation and down-regulation of p53, UPR and Nrf2-ARE pathways may be involved in the neuroprotective effect of luteolin.
    關聯: Plos One, v.9 n.5, e97880
    显示于类别:[藥學系(所)] 期刊論文
    [生物科技系(所)] 期刊論文

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