摘要
目的探讨一种长效环氧合酶-2(cyclooxygenase-2,Cox-2)抑制剂Mavacoxib(Trocoxil^(TM))对体外培养的人骨肉瘤细胞MG-63增殖和凋亡的影响及可能的作用机制。方法用MTT法检测不同浓度Mavacoxib在各时间点对MG-63细胞的生长抑制率,并观察其有效的作用浓度及作用时间;FCM法、Real-time PCR法和Western blot法分别检测Mavacoxib 50μmol/L干预MG-63细胞48小时后的细胞凋亡率及Cox-2、Bcl-2、Survivin和Bax的表达;Western blot检测Mavacoxib干预MG-63细胞后p-P38和P38蛋白的表达。结果 Mavacoxib可抑制MG-63细胞的增值(P<0.05);与空白对照组相比较,Mavacoxib干预组Bcl-2、Survivin下调,而Bax上调(P<0.05)。Mavacoxib干预MG-63细胞可促使P38信号通路蛋白的活化(P<0.05)。结论 Mavacoxib可通过抑制Cox-2、调节细胞凋亡因子及诱导P38通路的活化而抑制人骨肉瘤MG-63细胞。
Objective To investigate the effect of a long-acting cyclooxygenase-2 （Cox-2） inhibitor mavacoxib （ TrocoxilTM ） on proliferation and apoptosis of human osteosarcoma MG-63 cells, and its possible mechanism. Methods The inhibitory rates of proliferation of MG-63 cells after treatment with different concentrations of mavacoxib for different times were detec- ted by MTT assay. MG-63 cells after treatment with mavacoxib （50μmol/L）for 48 h, the apoptosis rates were detected by flow cytometry and the expression of Cox-2,Bcl-2,Survivin and Bax were detected by Real-time PCR and Western Blot;the proteins expression of p-P38 and P38 were detected by Western Blot. Results The proliferation inhibition rate of MG-63 cells in mavacoxib group were increased as compared with that in the blank group （without any treatment） （P 〈 0. 05 ）. The expression levels of Bcl-2 and Survivin in mavacoxib group were significantly down-regulated as compared with the blank group, whereas the Bax was up-regulated（ P 〈 0. 05）. The P38 pathway is activated （P 〈 0. 05 ）. Conclusion Mava- coxib inhibits human osteosarcoma MG-63 cells by inhibiting Cox-2,inducing the regulation factor of apoptosis and the acti- vation of P38 pathway.
出处
《世界科技研究与发展》
CSCD
2016年第1期131-135,共5页
World Sci-Tech R&D
基金
甘肃省创新研究群体计划项目(2013GS10047)资助
