MAPK信号转导系统在地塞米松诱导的CEM细胞增殖及凋亡中的作用

Mitogen-activated protein kinase mediates proliferation and apoptosis induced by dexamethasone in acute lymphoblastic leukemia cells

目的:探讨MAPK信号转导系统在地塞米松对CEM细胞增殖及凋亡中的作用。方法:台盼蓝拒染法测定增殖率;形态学及流式细胞仪解析细胞凋亡。结果:单用DEX培养24h-72h,细胞的增殖率分别为62.3%、35.5%、11.6%;SB203580预处理后,细胞的增殖率和单用DEX时相比分别升至82.8%、54.7%和48.1%(P<0.05);PD98059预处理后,,细胞的增殖率分别降至52.3%、19.8%和7.1%(P<0.05);SP600125预处理后,细胞的增殖率分别降至51.2%、19.5%和6.9%(P<0.05)。5μmol/LDEX处理CEM细胞36h时,亚二倍体细胞为26.2%,显著高于对照组(P<0.01)。SB203580预处理后,亚二倍体细胞由26.2%降至7.1%(P<0.01);PD98059预处理后,亚二倍体细胞升至38.6%(P<0.05),SP600125预处理后,亚二倍体细胞升至32.3%(P<0.05)。结论:MAPK信号转导通路参与地塞米松诱导的CEM细胞增殖及凋亡,表现为p38MAPK阻断增殖、促进细胞凋亡,ERK和JNK促进增殖、减少细胞凋亡。

Objective：To investigate the effect of mitogen -activated protein kinase on proliferation and apoptosis induced by dexamethasone in CEM cells. Methods： Cell viability was determined by trypan blue dye exclusion. Apoptosis was evaluated by morphology and flow cytometry. Results： Proliferation of dexamethasone - induced CEM cells was 62.3% ,35.5% and 11.6% at 24h,48h and 72h. Apoptotic percentage was 26.2% at 36h. When treatment with SB203580 and dexamethasone for 24h to 72h, the survival percentage was increased to 82.8% ,54.7% and 48.1%, respectively （P 〈 0.05 ）. Co - treatment with SB203580 and dexamethasone resulted in the decrease of apoptotic percentage to 7.1% at 36h（P 〈0.01 ）. When treatment with PD98059 and dexamethasone, the survival percentage was decreased to 52.3%, 19.8% and 7.1% , respectively （P 〈 0.05 ）. Cotreatment with PD9 80 5 9 and dexamethasone resulted in the increase of apoptotic percentage to 38.6% （P 〈0.05 ）. When treatment with SP600125 and dexamethasone, the survival percentage was decreased to 51.2% , 19.5% and 6.9%, respectively（ P 〈0.05）. Co-treatment with SP600 125 and dexamethasone resulted in the increase of apoptotic percentage to 32.3% （P 〈 O. 05 ）. Conclusion： Mitogen - activated protein kinase mediates proliferation and apoptosis induced by dexamethasone in CEM cells, p38MAPK inhibits CEM cells proliferation and enhances apoptosis, but ERK and JNK enhance proliferation and inhibit apoptosis.