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目的观察白细胞三烯(LTs)对食管癌Eca-109细胞株增殖的抑制作用及其对血管内皮生长因子(VEGF)的影响,探讨LTs在食道癌发生发展中的相关机制。方法将食管癌细胞Eca -109株传代培养,用非甾体类抗炎药物(NSIADs)阿司匹林及环氧合酶-2(COX-2)抑制剂NS-398作用该细胞株后,以ELISA法和细胞计数法测定食管癌细胞的LTD4(LTs的亚型)的浓度和细胞数;再将LTD4作用于癌细胞后,以同样方法检测癌细胞数和VEGF水平;MTT法测定LTs对人食管癌Eca- 109细胞增殖的抑制率。结果在阿司匹林(0．5-4．0mmol／L)和NS-398(25-200μmol／L)不同浓度的作用下,LTD4水平呈上升趋势,食管癌Eca-109细胞株生长受到不同程度的抑制,呈现浓度依赖性; LTD4对癌细胞的抑制作用随浓度升高而增强,并可明显降低VEGF水平。LTs受体拮抗剂孟鲁司特可有相反的作用。结论NSIADs在抑制COX-2途径的同时,促进了LTs的生成,从而抑制食管癌细胞的增殖及VEGF的生成,提示LTs可通过非COX-2途径在食管癌的发生发展中起重要作用。
Objective To investigate the inhibitory effect of leukotrienes (LTs) on the proliferation of esophageal carcinoma cell line Eca-109 and its effect on vascular endothelial growth factor (VEGF), and to explore the mechanism of LTs in esophageal carcinogenesis. Methods The esophageal cancer cell line Eca-109 was subcultured and treated with non-steroidal anti-inflammatory drugs (NSIADs) aspirin and cyclooxygenase-2 (NS-398) And cell count method to determine the esophageal cancer LTD4 (LTs subtype) concentration and cell number; then LTD4 role in cancer cells, the same method to detect the number of cancer cells and VEGF levels; MTT assay LTs on human esophageal cancer Inhibition of Eca-109 cell proliferation. Results The levels of LTD4 showed an upward trend under the different concentrations of aspirin (0.5-4.0mmol / L) and NS-398 (25-200μmol / L). The growth of Eca-109 cells was inhibited to some extent , Showing a concentration-dependent; LTD4 inhibition of cancer cells increased with increasing concentration, and can significantly reduce the level of VEGF. Montelukast, an LTs receptor antagonist, may have the opposite effect. Conclusions NSIADs can promote the production of LTs, inhibit the proliferation of esophageal cancer cells and the production of VEGF, simultaneously suggesting that LTs may play an important role in the pathogenesis of esophageal cancer through the non-COX-2 pathway.