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目的:研究选择性COX2抑制剂尼美舒利对低氧模拟剂氯化钴诱导的胃癌细胞株BGC823HIF1α、VEGF表达的影响。方法:分别应用150μmol/L氯化钴单独或联合10μmol/L、40μmol/L、80μmol/L的尼美舒利作用于BGC823细胞24h,收集细胞,应用RT PCR和Westernblot技术检测HIF1α及VEGF的表达。以胎牛血清加RPMI1640培养基培养细胞作正常对照。结果:与正常对照组比较,150μmol/L氯化钴刺激24h,可显著提高细胞HIF1α蛋白、VEGFmRNA和蛋白的表达(P<0.01),但对HIF1αmRNA表达无影响。与氯化钴单独作用比较,尼美舒利和氯化钴联合作用24h,细胞HIF1α蛋白、VEGFmRNA和蛋白表达降低(P<0.01),并呈剂量依赖性,但对HIF1αmRNA表达无影响。结论:COX2抑制剂尼美舒利可抑制氯化钴诱导的HIF1α、VEGF表达,这可能是其抗肿瘤血管生成的机制之一。
Objective: To investigate the effect of selective COX2 inhibitor nimesulide on the expression of BGC823HIF1α and VEGF in gastric cancer cell line BGC823 induced by hypoxia-mimics. Methods: BGC823 cells were treated with 150μmol / L cobalt chloride alone or in combination with 10μmol / L, 40μmol / L, 80μmol / L nimesulide for 24 hours. The expression of HIF1α and VEGF was detected by RT PCR and Western blotting . Fetal bovine serum plus RPMI1640 culture medium for normal control. Results: Compared with the normal control group, the stimulation of 150μmol / L cobalt chloride for 24 hours significantly increased the expression of HIF1α protein, VEGF mRNA and protein (P <0.01), but had no effect on the expression of HIF1α mRNA. Compared with cobalt chloride alone, nimesulide and cobalt chloride combined effect 24h, HIF1α protein, VEGF mRNA and protein expression decreased (P <0.01), and in a dose-dependent manner, but had no effect on HIF1αmRNA expression. Conclusion: Nimesulide, a COX2 inhibitor, inhibits the expression of HIF1α and VEGF induced by cobalt chloride, which may be one of the mechanisms of anti-tumor angiogenesis.