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目的研究环氧合酶(cyclooxygenase,COX)非选择性抑制剂布洛芬和COX-2选择性抑制剂氮-2,环己氧-4,硝基苯-甲级磺胺(NS398)对卵巢肿瘤血管形成的影响,并探讨其作用机制。方法2007年于北京协和医院,通过体外细胞共培养模型,观察COX抑制剂对人脐静脉内皮细胞(human umbilical vein endothelial cell,HUVEC)迁移能力的影响。采用逆转录聚合酶链反应(RT-PCR)检测COX抑制剂对OVCAR3血管内皮生长因子(vascularendothelial growth factor,VEGF)mRNA表达的影响。采用ELISA方法检测COX抑制剂对OVCAR3中VEGF和前列腺素E2(prostaglandin E2,PGE2)分泌的影响。结果两种COX抑制剂都能抑制HUVEC的迁移,抑制OVCAR3细胞中VEGF mRNA的表达和VEGF、PGE2的分泌。经NS398处理后,研究组HUVEC迁移细胞数目明显低于对照组[(39.0±3.8)个/400×视野vs(56.0±4.2)个/400×视野,P<0.05]。结论NS398和布洛芬通过抑制PGE2,在mRNA和蛋白水平下调VEGF的合成分泌,抑制血管内皮细胞的迁移。COX抑制剂可能成为干预卵巢肿瘤血管形成的一个新选择。
Objective To investigate the effect of ibuprofen, a selective inhibitor of cyclooxygenase (COX), and selective inhibitors of cyclooxygenase (COX-2) on ovarian cancer Vascular formation and explore its mechanism of action. Methods 2007 in Beijing Union Medical College Hospital, in vitro cell co-culture model to observe the COX inhibitor on human umbilical vein endothelial cells (human umbilical vein endothelial cell (HUVEC) migration ability. The effect of COX inhibitor on the expression of OVCAR3 mRNA was assayed by reverse transcription-polymerase chain reaction (RT-PCR). The effect of COX inhibitor on the secretion of VEGF and prostaglandin E2 (PGE2) in OVCAR3 was detected by ELISA. Results Both COX inhibitors could inhibit the migration of HUVEC and inhibit the expression of VEGF mRNA and the secretion of VEGF and PGE2 in OVCAR3 cells. After NS398 treatment, the number of HUVEC migrating cells in the study group was significantly lower than that in the control group [(39.0 ± 3.8) / 400 × vs (56.0 ± 4.2) / 400 × fields, P <0.05]. Conclusion NS398 and ibuprofen can inhibit the synthesis and secretion of VEGF at the mRNA and protein levels and inhibit the migration of vascular endothelial cells by inhibiting PGE2. COX inhibitors may be a new intervention in the intervention of ovarian tumor angiogenesis.