雷公藤内酯醇通过介导热休克蛋白27的表达诱导Hut78细胞凋亡

Triptolide induces apoptosis of Hut78 cells through inhibition of heat shock protein 27

目的:探讨雷公藤内酯醇(Triptolide,TP)诱导皮肤T细胞淋巴瘤Se’zary综合征Hut78的凋亡及机制。方法:采用MTT法检测Hut78细胞的增殖抑制率,Annexin V-FITC/PI双染流式细胞术检测Hut78细胞的凋亡率,Westernblot检测Hut78细胞中小分子热休克蛋白27(HSP27)的表达。结果:雷公藤内酯醇可诱导Hut78细胞凋亡(P<0.01),雷公藤内酯醇干预组,HSP27的表达被抑制。用p38MAPK特异性抑制剂SB203580干预后,雷公藤内酯醇诱导Hut78细胞凋亡率下降,HSP27的表达被抑制效应减弱。结论:雷公藤内酯醇可诱导Se’zary综合征细胞Hut78凋亡,该作用与抑制HSP27的表达密切有关,同时该作用可被p38MAPK特异性抑制剂SB203580显著抑制,提示p38MAPK信号通路也参与雷公藤内酯醇介导的Se’zary综合征细胞株Hut78中HSP27的表达。

Objective：To investigate the effect of triptolide on the apoptosis induction in Se＇zary Syndrome（SS） Hut78 cells,and the mechanism of this effect. Methods：The inhibitory effect of Hut78 cells was measured by MTT assay.The apoptosis rate of Hut78 cells was assessed by Annexin V-FITC/PI Heat shock protein 27 was determined by Western blot analysis.Results：Triptolide induced apoptosis of Hut78 cells and apparently inhibited the expression of HSP27 in Hut78 cells（P0.01）.However,after interference with p38MAPK inhibitor（SB203580）,the inhibitory effect of triptolide on Hut78 cells was significantly weakened.Conclusions：Triptolide induces apoptosis of Hut78 cells partly by inhibition of HSP27,The effects are mediated,at least in part,through the activation of P38MAPK signaling pathway