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目的探讨细胞内细胞色素氧化酶 p45 0 (CYP)表达、视黄酸 (RA)代谢与细胞凋亡的相互关系。方法采用脂质体介导的质粒转染和逆转录 - PCR等实验技术方法做有关分析检测。结果野生型 HL- 6 0细胞 hp45 0 RAI表达微弱 ,脂质体介导的 hp45 0 RAI质粒转染可使 HL- 6 0细胞稳定表达 hp45 0 RAI;hp45 0 RAI转染对 ATRA诱导的 HL- 6 0细胞增殖能力无明显影响 ;野生型 HL- 6 0细胞有较强 Bcl- 2表达 ,ATRA处理抑制未转染细胞 Bcl- 2表达 ,但单纯 hp45 0 RAI转染、hp45 0 RAI转染 +CYP抑制剂或加用 IFN- α均能增强 Bcl- 2表达 ,其中以加用 ketoconazole作用更为显著。结论 RA敏感 HL- 6 0细胞中影响 RA代谢的主要 CYP并非 hp45 0 RAI,hp45 0 RAI转染能增强 Bcl- 2表达 ,但对 HL - 6 0细胞增殖能力无明显影响 ,CYP抑制剂、IFN-α可能通过抑制细胞内 RA代谢 ,而增加 HL - 6 0细胞Βcl- 2表达。
Objective To investigate the relationship between intracellular cytochrome oxidase p45 0 (CYP) expression and retinoic acid (RA) metabolism and apoptosis. Methods Liposome - mediated plasmid transfection and reverse transcription - PCR and other experimental techniques to do the analysis of detection. Results The expression of hp45 0 RAI in wild-type HL-60 cells was weak, and hp45 0 RAI was stably expressed in HL-60 cells by liposome-mediated hp45 0 RAI plasmid transfection. The effect of hp45 0 RAI on ATRA-induced HL- 6 0 cell proliferation had no significant effect; wild-type HL-60 cells have strong Bcl-2 expression, ATRA treatment inhibited untransfected cells Bcl-2 expression, but hp45 0 RAI transfection, hp45 0 RAI transfection + CYP inhibitors or IFN-α plus can enhance the expression of Bcl-2, which ketoconazole role with more significant. CONCLUSION: The main CYP affecting RA metabolism in RA sensitive HL-60 cells is not hp45 0 RAI. The hp45 0 RAI transfection can enhance the expression of Bcl-2, but has no obvious effect on the proliferation of HL-60 cells. CYP inhibitor, IFN -α may increase the expression of Bcl-2 in HL - 60 cells by inhibiting the intracellular RA metabolism.