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首页> 外文期刊>Journal of Cellular Physiology >Quercetin Partially Preserves Development of Osteoblast Phenotype in Fetal Rat Calvaria Cells in an Oxidative Stress Environment
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Quercetin Partially Preserves Development of Osteoblast Phenotype in Fetal Rat Calvaria Cells in an Oxidative Stress Environment

机译：槲皮素部分保护的发展在胎鼠头顶细胞成骨细胞表型在氧化应激环境中

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Studies are needed to improve understanding of the osteoblast antioxidant response, and the balance between oxidative homeostasis and osteoblast differentiation. The flavonol quercetin aglycone (QRC) up-regulates the osteoblast antioxidant response in vitro without suppressing osteoblast phenotype, suggesting that QRC may preserve osteoblast phenotypic development in cells subsequently exposed to oxidative stress, which suppresses osteoblast differentiation. The aims of this study were to assess the extent that QRC pretreatment preserved development of the osteoblast phenotype in cells subsequently cultured with hydrogen peroxide, an oxidative stressor, and to characterize alterations in the osteoblast antioxidant response and in key antioxidant signaling pathways. We hypothesized that pretreatment with QRC would preserve phenotypic development after hydrogen peroxide treatment, suppress the hydrogen peroxide-induced antioxidant response, and that the antioxidant response would involve alterations in Nrf2 and ERK1/2 signaling. Results showed that treating fetal rat calvarial osteoblasts for 4 days (D5-9) with 300 mu M hydrogen peroxide resulted in fewer alkaline phosphatase-positive cells and mineralized nodules, altered cell morphology, and significantly lower osteoblast phenotypic gene expression (P<0.05). This suppression was partially blocked when cells were pretreated 12 h with 20 mM QRC. Hydrogen peroxide also produced sustained up-regulation of heme oxygenase-1 (HO-1) and g-glutamate cysteine ligase catalytic subunit (GCLC), which was partially blocked in hydrogen peroxide-treated cells that first received QRC pretreatment. The alterations in the antioxidant stress response coincided with alterations in phosphorylated ERK1/2, but not Nrf2. These results suggest that QRC suppresses hydrogen peroxide-induced activation of the antioxidant response, and partially preserves osteoblast phenotypic development. (C) 2016 Wiley Periodicals, Inc.
机译：研究需要改进的理解成骨细胞抗氧化反应和平衡氧化体内平衡和成骨细胞之间分化。(独有)让成骨细胞抗氧化剂反应没有抑制成骨细胞的体外表型,这表明独有的保佑细胞的成骨细胞表型发展随后暴露于氧化应激,抑制成骨细胞分化。本研究评估,独有的预处理保存的发展在随后的细胞成骨细胞表型培养与过氧化氢氧化压力源,和描述的更改成骨细胞抗氧化反应和关键抗氧化信号通路。预处理与独有的保护过氧化氢后表型发展治疗,抑制氢peroxide-induced抗氧化反应,抗氧化剂反应需要在Nrf2和改变ERK1/2信号。胎鼠颅顶的成骨细胞为4天(D5-9)与300μM过氧化氢导致更少碱性phosphatase-positive细胞和矿化结节,细胞形态学改变显著降低成骨细胞表型的基因表达(P < 0.05)。当细胞被12 h预处理部分屏蔽20毫米独有的。血红素oxygenase-1持续上调(HO-1)和g-glutamate半胱氨酸连接酶催化亚基(GCLC),部分屏蔽氢peroxide-treated细胞收到独有的预处理。抗氧化应激反应同时发生在磷酸化ERK1/2改变,但不是Nrf2。氢peroxide-induced激活的抗氧化反应,部分保留成骨细胞表型的发展。期刊、公司。

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