雷公藤诱导皮肤T细胞淋巴瘤Hut102的凋亡及机制  

Triptolide induces apoptosis of Hut102 cells through p38 MAPK pathway

作　　者：谢会霞[1] 郝进[1] 

机构地区：[1]重庆医科大学附属第二医院皮肤科,重庆400010

出　　处：《中国现代医学杂志》2010年第18期2770-2774,共5页China Journal of Modern Medicine

摘　　要：目的探讨雷公藤内酯醇(TP)诱导皮肤T细胞淋巴瘤Hut102细胞株的凋亡及机制。方法采用MTT法检测Hut102细胞的增殖抑制率,Annexin v-FITC/PI双染流式细胞术检测Hut102细胞的凋亡率,Western印迹法检测Hut102细胞中磷酸化p38丝裂原活化蛋白激酶(p38MAPK)、caspase-3、热休克蛋白27(Hsp27)的表达。结果雷公藤内酯醇可诱导Hut102细胞凋亡(P<0.01),磷酸化p38MAPK、caspase-3被激活,同时抑制Hsp27的表达。用p38MAPK特异性抑制剂SB203580干预后,雷公藤内酯醇诱导Hut102细胞凋亡率下降,磷酸化p38的表达降低,caspase-3激活被抑制,Hsp27的表达增加。结论雷公藤内酯醇可诱导Hut102细胞凋亡,该作用可被p38MAPK特异性抑制剂SB203580显著抑制,提示雷公藤内酯醇可能通过激活p38MAPK信号通路使部分Hut102细胞产生凋亡。【Objective】 To investigate the effect of triptolide on the apoptosis induction in human cutaneous T-cell lymphoma Hut102 cells,and the mechanism of this effect.【Methods】The inhibitory effect of Hut102 cells was measured by MTT assay.The apoptosis rate of Hut102 cells was assessed by Annexin v-FITC/PI.Expression of phosphorylated p38 Mitogen-activated protein kinase kinases（p-p38MAPK）,caspase-3 and Heat shock protein 27（Hsp27） were determined by Western blot analysis.【Results】Triptolide induced apoptosis of Hut102 cells and apparently increased the activity of p-p38 MAPK and caspase-3,inhibited the expression of Hsp27 in Hut102 cells（P 0.01）.However,after interference with p38MAPK inhibitor（SB203580）,the inhibitory effect of triptolide on Hut102 cells was significantly weakened.The apoptosis rate of the cells,the activity of p-p38MAPK,caspase-3 and the inhibition of Hsp27 also decreased dramatically.【Conclusions】Triptolide could induce apoptosis of Hut102 cells.The effect could be markedly suppressed by p38MAPK inhibitor（SB203580）.Triptolide induced apoptosis of Hut102 cells partly by activating p38 MAPK.

关 键 词：雷公藤内酯醇 Hut102 P38MAPK 热休克蛋白27 细胞凋亡 

分 类 号：R739.5[医药卫生—肿瘤]