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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/17336

    Title: Protection by chrysin, apigenin, and luteolin against oxidative stress is mediated by the Nrf2-dependent up-regulation of heme oxygenase 1 and glutamate cysteine ligase in rat primary hepatocytes
    Authors: Chin-Shiu Huang;Chong-Kuei Lii;Ai-Hsuan Lin;Yu-Wen Yeh;Hsien-Tsung Yao;Chien-Chun Li;Tsu-Shing Wang;Haw-Wen Chen
    Contributors: 保健營養生技學系
    Keywords: Extracellular signal-regulated protein kinase 2 (ERK2);Flavones;Heme oxygenase 1 (HO-1);Glutamate cysteine ligase (GCL);Nuclear factor erythroid 2-related factor 2 (Nrf2)
    Date: 2012-08
    Issue Date: 2012-11-26 10:31:40 (UTC+8)
    Abstract: Chrysin, apigenin, and luteolin are flavones that differ in their number of hydroxyl groups in the B ring. In this study, we investigated the protection by chrysin, apigenin, and luteolin against tert-butyl hydroperoxide (tBHP)-induced oxidative stress and the possible mechanisms involved in rat primary hepatocytes. Chrysin, apigenin, and luteolin dose-dependently up-regulated the protein expression of heme oxygenase 1 (HO-1) and glutamate cysteine ligase (GCL) catalytic (GCLC) and modifier subunit (GCLM) and increased the intracellular glutathione (GSH) content and the ratio of GSH to oxidized GSH. Among the flavones studied, chrysin showed the greatest induction of HO-1, GCLC, and GCLM protein expression and GSH content. Cellular reactive oxygen species production induced by tBHP was attenuated by pretreatment with chrysin, apigenin, and luteolin (P < .05), and this protection was reversed by the GCL inhibitor l-buthionine-S-sulfoximine and the HO-1 inhibitor zinc protoporphyrin. Chrysin, apigenin, and luteolin activated extracellular signal-regulated protein kinase 2 (ERK2), nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation, nuclear Nrf2–antioxidant responsive element (ARE) binding activity, and ARE-dependent luciferase activity. Both ERK2 and Nrf2 siRNAs attenuated chrysin-induced HO-1, GCLC, and GCLM protein expression. Taken together, these results suggest that chrysin, apigenin, and luteolin inhibit tBHP-induced oxidative stress by up-regulating HO-1, GCLC, and GCLM gene transcription via the ERK2/Nrf2/ARE signaling pathways in rat primary hepatocytes.
    Relation: ARCHIVES OF TOXICOLOGY, 87(1):167-178.
    Appears in Collections:[食品營養與保健生技學系] 期刊論文

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