雷公藤红素诱导CEM-6T细胞凋亡的机制研究

Study on the Mechanism of Apoptosis in Human Cell Line CEM-6T Induced by Tripterine

在已经证明雷公藤红素能诱导人T淋巴细胞株CEM 6T细胞凋亡的基础上 ,进一步探讨此凋亡过程的机制。本项目研究雷公藤红素诱导CEM 6T细胞凋亡过程中Fas/FasL、ICEmRNA的变化以及ICE抑制剂、磷酸酶抑制剂对凋亡的影响。结果发现 ( 1)CEM 6T细胞表达Fas,不表达FasL ,雷公藤红素处理不能改变这一情况 ;( 2 )雷公藤红素不能改变ICEmRNA的表达水平 ,但ICE抑制剂Ac YVAD CHO能使雷公藤红素诱导CEM 6T的凋亡率下降 ;( 3) 1 5 μmol/L磷酸酶抑制剂okadaicacid能使凋亡率下降。提示雷公藤红素诱导CEM 6T细胞凋亡不依赖Fas/FasL ,而与细胞内原已存在的ICE有关 。

On the basis of the effect of Tripterine to induce apoptosis in human T cell line CEM 6T,the mechanism of the apoptoticprocess was further investigated to explore the changes of Fas/FasL,ICE mRNA and the effect of ICE inhibitor as well as phosphatase inhibitor It was found that Fas was expressed on the CEM 6T cells, while no expression of FasL was found on these cells,which could not be altered by the treatment with Tripterine Both ICE inhibitor Ac YVAD CHO and 1 5 mol/L of protein phosphatase inhibitor okadaic acid could decrease the apoptotic rates of CEM 6T cells induced by Tripterine These results suggest that the induction of apoptosis in CEM 6T cells is Fas/FasL interaction independent but associated with the intracellular pre existence of ICE It suggests that protein phosphatase might participate in the apoptotic process