昆明山海棠碱通过Fas受体介导途径诱导Jurkat淋巴瘤细胞株凋亡

目的 探讨Fas、caspase-8在昆明山海棠碱(THH碱)对Jurkat淋巴瘤细胞的凋亡诱导中的变化，以进一步研究THH碱诱导凋亡的分子机制。方法 采用Annexin—Ⅴ标记和流式细胞术检测细胞的凋亡发生率，采用western blotting分析FasL、caspase-7、caspase-8、Bid等蛋白表达的变化。结果 THH碱能有效诱导Jurkat细胞凋亡；在其凋亡过程中，FasL逐渐表达增强、caspase-7、caspase-8、Bid剪切激活，并呈时间依赖性。结论 THH碱通过Fas受体—配体介导激活caspase-8，caspase-8再激活caspase-7和Bid等网络途径诱导Jurkat细胞凋亡。

Tripterygium hypoglaucum (Levl) Hutch alkaloids induce apoptosis of Jurkat lymphoma cells via the Fas receptor-mediated pathway

Objective To explore the changes of Fas ligand (FasL) and caspase 8 during the apoptotic process of human lymphoma Jurkat T cells induced by Tripterygium hypoglaucum (Levl) Hutch (THH) alkaloids to study the molecular mechanisms of the apoptosis. Methods After Jurkat cells were induced by THH alkaloids, translocated phosphatidylserine was labeled with Annexin V Fluorescence; the apoptotic incidence was measured by flow cytometry; changes of the expressions of FasL, Bid, caspase 7 and caspase 8 proteins were determined by Western blotting. Results THH alkaloids could effectively induce the apoptosis of Jurkat cells. FasL expression was increased and caspase 8, caspase 7 and Bid were activated in a time dependent manner after treatment with THH alkaloids. Conclusion THH alkaloids induce the apoptosis of Jurkat cells via the activation of caspase 7 and Bid through the FasL mediated activation of caspase 8.