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炎症在肿瘤的发生发展过程中扮演重要角色,脂氧素是一类重要的内源性抗炎介质。但是迄今为止,脂氧素对肿瘤的影响报道极少。为此,本文研究了脂氧素对HL-60和K562白血病细胞增殖和凋亡的影响。体外培养白血病细胞株HL-60和K562,Western印迹和实时荧光定量PCR检测脂氧素受体的表达情况;CCK-8法(cell counting kit-8 assay)检测HL-60和K562的增殖能力;PI染色后利用流式细胞仪进行细胞周期分析;膜联蛋白V试剂盒检测脂氧素对细胞凋亡的影响。实验结果表明脂氧素抑制HL-60和K562白血病细胞增殖(P<0.05);脂氧素处理组S期细胞比例明显减少而G_0/G_1期细胞比例增加;脂氧素还可以诱导HL-60和K562白血病细胞凋亡。由此可见,脂氧素抑制HL-60和K562白血病细胞增殖,其机制可能与诱导白血病细胞G_0/G_1期阻滞和细胞凋亡有关。
Inflammation plays an important role in tumorigenesis and development. Lipoxin is an important class of endogenous anti-inflammatory mediators. But so far, the impact of lipoxin on tumors is rarely reported. Therefore, we studied the effects of lipoxin on the proliferation and apoptosis of HL-60 and K562 leukemia cells. The leukemia cell lines HL-60 and K562 were cultured in vitro. The expression of lipoxin receptor was detected by Western blotting and real-time fluorescence quantitative PCR. The proliferation of HL-60 and K562 cells was detected by CCK-8 assay. Cell cycle analysis was performed by flow cytometry after PI staining. Annexin V kit was used to detect the effect of lipoxin on apoptosis. The results showed that lipoxin could inhibit the proliferation of HL-60 and K562 leukemia cells (P <0.05). The proportion of cells in S phase and the percentage of cells in G 0 / G 1 phase increased significantly in lipoxin treatment group. Lipoxygen could also induce HL-60 And K562 leukemia cells. Thus, lipoxin can inhibit the proliferation of HL-60 and K562 leukemia cells, the mechanism may be related to the induction of G 0 / G 1 phase arrest and apoptosis in leukemia cells.