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目的 观察5-脂氧合酶拮抗剂MK886、环氧化酶2拮抗剂Celeeoxib干预SW1990细胞后对细胞增殖及血管内皮生长因子(VEGF)mRNA表达的影响.方法 应用不同浓度的MK886、Celecoxib 以及两者联合处理SW1990细胞,采用胆囊收缩素(CCK-8)法检测细胞的增殖,RT-PCR法检测细胞白三烯B4受体1(BLT1) mRNA、前列腺素2(PGE2) mRNA、VEGF mRNA的表达.结果 10μmol/LMK886或20 mmol/L Celecoxib处理24h后,SW1990细胞的增殖受到明显抑制(1.80±0.06比1.65±0.10;2.04 ±0.03比1.86 ±0.02,P＜0.05),且随药物浓度的增加,细胞的增殖抑制更明显.两拮抗剂联合干预12h后,SW1990细胞的增殖即受到非常明显的抑制(1.72±0.05比1.52±0.05,P＜0.01).Celecoxib处理细胞48 h后,细胞BLT1、VEGF mRNA表达与对照组比较无明显变化,但PGE2 mRNA的表达明显减少(37.50比71.50,P＜0.05)；MK886或MK886+ Celecoxib联合处理细胞后,细胞BLT1、VEGF mRNA表达明显减少(40.30、22.75比126.50,P＜0.05),而PGE2 mRNA的表达与对照组比较无明显变化.结论 花生四烯酸的两条代谢途径均与胰腺癌的发生及增殖有密切关系,同时抑制两条途径可显著抑制胰腺癌细胞的增殖.

Objective To investigate the effects of two inhibitors of arachidonic acid metabolic pathway (5-cyclooxygenase blockade MK886 and COX 2 blockade celecoxib) on growth and VEGF mRNA expression of human pancreatic cancer cell SW1990.Methods Pancreatic cancer cells SW1990 were cultured with different concentrations of MK886,celecoxib,MK886 and celecoxib,then the cell proliferation was detected by using CCK-8,BLT1 mRNA,PGE2 mRNA and VEGF mRNA expressions were determined by RTPCR.Results After 10 μmol/L MK886 or 20 mmol/L celecoxib treatment for 24 h,the growth of SW1990 was greatly suppressed ( 1.80 ±0.06 vs 1.65 ±0.10,2.04 ±0.03 vs 1.86 ±0.02,P ＜0.01 ),and the growth suppression of SW1990 cells was increased accompanying the raised concentration of MK886 or celecoxib.After both MK886 and celecoxib treatment for 12 h,the growth of SW 1990 cells was much obviously suppressed (1.72 ±0.05 vs 1.52 ±0.05,P ＜0.01 ).After celecoxib treatment for 48 h,the BLT1 mRNA,PGE2 mRNA and VEGFmRNA expressions were not significantly changed,but the expressions of PGE2 mRNA were significantly decreased ( P ＜ 0.05 ).After MK886 or MK886 + celecoxib treatment,the expressions of BLT1 mRNA,VEGF mRNA were significantly decreased ( P ＜ 0.05 ),but the expressions of PGE2 mRNA were not significantly changed when compared to control group.Conclusions Two metabolic pathways of arachidonic acid have a close relation with occurrence and proliferation of pancreatic cancer,when both of the pathways were blocked,the proliferation of the pancreatic cancer cell was suppressed obviously.