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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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Effect of Clenbuterol Hydrochloride on the in vitro Development of Mouse Embryo

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Journal of Reproduction and Contraception 2002年第3期13卷 146-151页

作者： Li-huaLU Wei-jieZHU JingLI CenterforReproductiveImmunologyResearch JinanUniversityGuangzhou510632China dept.ofpathophysiology MedicalCollegeJinanUniversityGuangzhou510632China

To investigate the effect of clenbuterol hydrochloride on the in vitro development of both 1 cell and 2 cell mouse embryos. Methods The cultural systems of both 1 cell and 2 cell mouse embryo were used to determine the effect of clenbuterol hydrochloride at doses of 1 ng/mL, 3 ng/mL, and 10 ng/mL on developmental rates of mouse embryos. Results When 1 cell embryos cultured with 1 ng/mL of clenbuterol hydrochloride, developmental rates from the 4 cell stage to blastocyst stage were significantly lower than those in the control group (P0.05). However, at levels of 3 ng/mL and 10 ng/mL, significant decrease of developmental rates in 2 cell embryos was observed from the 4 cell and from the 8 cell stage, respectively (P<0.05). Embryos cultured with clenbuterol hydrochloride appeared to have more granules, fragments and degeneration than those in the control. Conclusion Clenbuterol hydrochloride has a toxic effect on the mouse embryos, and the effect is in a dose dependent. 1 cell mouse embryos cultured with clenbuterol hydrochloride could be easily inhibited at 2 cell stage, but the effect of clenbuterol hydrochloride on development of the late 2 cell embryos would be reduced.

关键词： clenbuterol hydrochloride mouse embryo in vitro culture

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Assay of sIL-2R and TNF-α in experimental allergic encephalomyelitis

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白求恩医科大学学报 2001年第4期27卷 339-343页

作者： WANGLin HUAKun 等 dept.ofNeurology FirstHospitalJilinUniversityChangchun130021China dept.ofpathophysiology SchoolofBa

目的 :研究 s IL- 2 R和 TNF- α在实验性变态反应性脑脊髓炎 (EAE)免疫发病机制中的变化与作用。方法 :应用豚鼠诱导 EAE动物模型。在 MBP+CFA免疫豚鼠的第 8、15、2 2天处死动物 ,取脾细胞 ,加入 Con A诱生培养 ,收集上清液 ,采用 EL... 详细信息

目的 :研究 s IL- 2 R和 TNF- α在实验性变态反应性脑脊髓炎 (EAE)免疫发病机制中的变化与作用。方法 :应用豚鼠诱导 EAE动物模型。在 MBP+CFA免疫豚鼠的第 8、15、2 2天处死动物 ,取脾细胞 ,加入 Con A诱生培养 ,收集上清液 ,采用 ELISA方法测定 s IL- 2 R水平 ,采用生物活性测定法检测TNF- α水平。结果 :EAE组的 s IL- 2 R与 TNF- α水平明显高于正常对照组。结论 :s IL- 2 R及 TNF-

关键词：变态反应性脑脊髓炎 EAE 动物模型 sIL-2R TNFα MS

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