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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 ,蛋白去磷酸化参与了此凋亡过程
It has been demonstrated that tripterine can induce apoptosis of human T lymphocyte cell line CEM 6T cells and further explore the mechanism of this apoptotic process. This project studied the changes of Fas/FasL and ICE mRNA in the apoptosis of CEM 6T cells induced by tripterine and the effects of ICE inhibitors and phosphatase inhibitors on apoptosis. The results showed that (1) CEM 6T cells expressed Fas and did not express FasL, and tripterine treatment could not change this condition; (2) Tripterine did not change the expression level of ICE mRNA, but the ICE inhibitor Ac YVAD CHO could make Lei Gong. Gentin induces a decrease in the apoptosis rate of CEM 6T; (3) The okadaicacid, a 15 μmol/L phosphatase inhibitor, can reduce the apoptosis rate. It is suggested that the apoptosis of CEM 6T cells induced by tripterine does not depend on Fas/FasL but is related to the ICE that is already present in the cell. Dephosphorylation of the protein participates in this process of apoptosis.