论文部分内容阅读
学教研室,公共卫生学院,第一附属医院,广西南宁530021;[摘要]目的:研究苯的代谢产物氢醌(HQ)对HL-60细胞TNF-α产生和细胞活性的影响,并探讨这种影响是否通过氧化还原调节来实现。方法:HL-60细胞用不同浓度HQ刺激24h后,收集细胞及培养液上清,检测细胞内活性氧、氧化型/还原型谷胱甘肽含量,CCK8检测细胞增殖,流式细胞术(FCM)检测细胞凋亡,ELISA法检测TNF-α含量。结果:5μmol/LHQ即可诱导GSH水平增高,抑制HL-60细胞增殖,但对GSH/GSSG比例,TNF-α表达及细胞凋亡无显著影响。50、100μmol/LHQ可破坏细胞内氧化还原状态,GSH/GSSG比例下降,TNF-α表达增高,显著抑制HL-60细胞增殖,诱导细胞凋亡,抗氧化剂N-乙酰半胱氨酸能拮抗HQ诱导的TNF-α表达、增殖抑制及细胞凋亡。结论:HQ可通过改变HL-60细胞内氧化还原状态诱导TNF-α表达,导致细胞凋亡。
To investigate the effect of benzene hydroquinone (HQ) on TNF-α production and cell viability in HL-60 cells, and to explore whether this kind of Whether the impact is achieved through redox regulation. Methods: HL-60 cells were stimulated with different concentrations of HQ for 24 hours. The supernatant of cells and culture supernatants were collected. The levels of reactive oxygen species (ROS) and oxidized / reduced glutathione (GSH) were measured. The proliferation of cells was detected by flow cytometry ) To detect apoptosis, ELISA method for detecting TNF-α content. Results: 5μmol / LHQ could increase the level of GSH, inhibit the proliferation of HL-60 cells, but had no significant effect on the ratio of GSH / GSSG, the expression of TNF-α and apoptosis. 50, 100μmol / LHQ could destroy intracellular redox state, GSH / GSSG ratio decreased, TNF-α expression increased significantly inhibited HL-60 cell proliferation, induced apoptosis, antioxidant N-acetylcysteine can antagonize HQ Induced TNF-αexpression, proliferation inhibition and apoptosis. CONCLUSION: HQ can induce TNF-α expression by changing the redox state in HL-60 cells, resulting in apoptosis.