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毒理学杂志 2001年第2期15卷 106-106页

作者：夏小俊金中初浙江大学医学院病理生理教研室!杭州310006

酪醇对肝癌细胞nq01的诱导及细胞增殖的抑制

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毒理学杂志 2001年第2期15卷 106-106页

作者：薛丽君金中初浙江大学医学院病理生理教研室!310006

Sulforaphane Protects Astrocytes Against Oxidative Stress and Delayed Death Caused by Oxygen and Glucose Deprivation

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神经损伤与功能重建 2009年第2期4卷 114-124,135页

作者： CAMELIA A.DANILOV KRISH CHANDRASEKARAN JENNIFER RACZ LUCIAN SOANE CAROL ZIELKE AND GARY FISKUM Department of Anesthesiology University of Maryland School of Medicine Program in Neuroscience University of Maryland School of Medicine Department of Pediatrics University of Maryland School of Medicine rauma and Anesthesiology Research Center University of Maryland School of Medicine

氧化应激是缺血再灌注后星形胶质细胞损伤和死亡的重要分子机制之一,可能成为有效的干预靶点。下述治疗策略可减轻缺血再灌注条件下产生的多种反应性氮氧化合物损伤。这种方法可通过使用化学试剂或适当条件促进转录活化因子NRF2从细胞... 详细信息

氧化应激是缺血再灌注后星形胶质细胞损伤和死亡的重要分子机制之一,可能成为有效的干预靶点。下述治疗策略可减轻缺血再灌注条件下产生的多种反应性氮氧化合物损伤。这种方法可通过使用化学试剂或适当条件促进转录活化因子NRF2从细胞浆转入细胞核,并与抗氧化基因反应位点结合,来诱导缺血再灌注后损伤细胞的Ⅱ期基因反应。本研究将验证如下假说:NRF2基因表达通路激活剂sulforaphane能对体外无氧无糖环境处理的培养皮质星形胶质细胞起神经保护作用。将皮质星形胶质细胞暴露于无氧无糖环境(OGD)4 h,于干预前48 h或干预后给予5μMsulforaphane(NRF2基因表达通路激活剂)培养48 h,两种培育条件下细胞死亡均明显减少。免疫细胞化学结果表明干预前给予sulforaphane处理,细胞中DNA/RNA氧化标志物8-hydroxy-2-deox-yguanosine的表达在恢复给氧4 h后降低,两种培育条件下胞浆内及胞核内NRF2的免疫反应均增强且nqO1(NRF2转录活化基因产物)的表达和酶活性均增强。本研究提示sulforaphane可通过激活NRF2抗氧化基因表达通路,减少体外缺氧再灌注后星形胶质细胞的死亡。

关键词：缺氧再灌注 NRF2 nq01 氧化应激 8-hydroxy 2 deoxyguanosine

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Antioxidant and hypoxia induce the human antioxidant response element-mediated expression of NAD(P)H:quinone oxidoreductase1 gene

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癌变．畸变．突变 2001年第4期13卷 227-228页

作者： Lijun Xue Zhongchu Jin Dept.ofPathophysiology ZhejiangUniversitySchoolofMedicineHangzhouZhejiangPeoplesRepofChina310031 D

Background: NAD(P)H: quinone oxidoreductase 1 (nqO1) is an obligate two-electron reductase that is involved in protection of cells against redox cycling, oxidative stress, and neoplasia. and can also bioactivate certain antitumor quinones. Many antioxidants are cancer chemopreventive agents, and tumour hypoxia are now being exploited in cancer treatment which shows considerable promise to overcome the resistance to cancer chemotherapy. Antioxidant response element (ARE) is sensitive to perturbations of cellular redox states. Our previous studies have shown that β-tyrosol (β-TY), as a phenolic antioxidant, can protects cells against DNA damage resulting from toxic H2O2. Aim: We take the present study with the goal of whether antioxidants such as β-tyrosol, butylated hydroxyanisole(BHA) and β-Naphthooflavone(β-NF) and hypoxia (pO2 0.1% -0.5%) can induce gene expression of nqO1, inhibit proliferation of human hepatoma cells SMMC-7721 and the relationship between them; whether ARE can mediate gene expression in response to antioxidans and hypoxia. Methods: SMMC-7721 human hepatoma cells are planted in plates, grown for 24h. and exposed to antioxidants and hypoxia, each alone or in combination for another 24h. The enzyme activity was determinied by spectrophotometric assay using direct measurement of nqO1 from cells cultured in Microtiter wells. Semi-quantitative reverse transcription-PCR (RT-PCR) technique was used to measure nqO1 mRNA levets. Proliferation was estimated using the crystal violet staining technique. Electrophoretic mobility shift assay (EMSA) was employed to assess protein binding to the ARE under all of These conditions. Hypoxia cells were harvested in an anaerobic chamber at the end of the incubation period. Results: Antioxidant (90ug/ml β-TY、60μmol/L BHA、80μmol/L β-NF) potently induce an increase in the activity of nqO1. From 60μg/ml to 90μg/ml, β-TY caused nqO1 activity enhancement in a dose-dependent manner The nqO1 activity induced by 80μg/ml β-TY

关键词：肝脏肿瘤 NADH nq01 基因表达抗氧化剂低氧

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USING BIOM ARKERS TO IMPROVE BENZENE RISK ASSESSMENT AND FIND THE CAUSES OF LEUKAEMIA

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癌变．畸变．突变 2001年第4期13卷 212-212页

作者： Martyn T.Smith School of

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