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báo cáo khoa học: " Regulation of hypoxia inducible factor-1a expression by the alteration of redox status in HepG2 cells"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Regulation of hypoxia inducible factor-1a expression by the alteration of redox status in HepG2 cells | Jin et al. Journal of Experimental Clinical Cancer Research 2011 30 61 http www.jeccr.eom content 30 1 61 Journal of Experimental Clinical Cancer Research RESEARCH Open Access Regulation of hypoxia inducible factor-1 a expression by the alteration of redox status in HepG2 cells Wen-sen Jin1 Zhao-lu Kong2 Zhi-fen Shen2 Yi-zun Jin2t Wu-kui Zhang1 and Guang-fu Chen1 Abstract Hypoxia inducible factor-1 HIF-1 has been considered as a critical transcriptional factor in response to hypoxia. It can increase P-glycoprotein P-Gp thus generating the resistant effect to chemotherapy. At present the mechanism regulating HIF-1a is still not fully clear in hypoxic tumor cells. Intracellular redox status is closely correlated with hypoxic micro-environment so we investigate whether alterations in the cellular redox status lead to the changes of HIF-1a expression. HepG2 cells were exposed to Buthionine sulphoximine BSO for 12 h prior to hypoxia treatment. The level of HIF-1a expression was measured by Western blot and immunocytochemistry assays. Reduce glutathione GSH concentrations in hypoxic cells were determined using glutathione reductase 5 5-dithiobis- 2-nitrob-enzoic acid DTNB recycling assay. To further confirm the effect of intracellular redox status on HIF-1a expression N-acetylcysteine NAC was added to culture cells for 8 h before the hypoxia treatment. The levels of multidrug resistance gene-1 MDR-1 and erythropoietin EPO mRNA targeted by HIF-1a in hypoxic cells were further determined with RT-PCR and then the expression of P-Gp protein was observed by Western blotting. The results showed that BSO pretreatment down-regulated HIF-1a and the effect was concentration-dependent on the other hand the increases of intracellular GSH contents by NAC could partly elevate the levels of HIF-1a expression. The levels of P-Gp MDR-1 and EPO were concomitant with the trend of HIF-1a expression. Therefore our data indicate that the changes of redox status in hypoxic cells may regulate .