目的 · 探讨藤黄酸（GA）对NK/T 细胞淋巴瘤（NK/TCL）细胞株SNK-1、SNK-6 和 SNT-8 诱导凋亡的作用及其可能机制。 方法 · 以不同浓度GA 处理SNK-1、SNK-6 和 SNT-8 细胞株24 h，CCK-8 法测定GA 对细胞活力的影响；Annexin V-FITC/PI 流式细 胞术检测细胞凋亡；Western blotting 方法检测凋亡和信号通路相关蛋白及磷酸化的变化。结果 · CCK-8 法检测结果显示GA 对 3 株 细胞活力均有显著抑制作用。流式细胞术检测结果显示，GA 诱导 3 株细胞凋亡。Western blotting 检测结果显示 GA 处理的细胞出现 caspase-3 和 caspase-9 的活化及PARP 的剪切，且Bcl-xl 表达下降。信号通路蛋白STAT3 的磷酸化水平在SNK-1 和 SNT-8 中显著下 调，ERK1/2 的磷酸化水平在 SNK-1 和 SNK-6 中显著下调。结论 · GA 对 NK/TCL 细胞株 SNK-1、SNK-6 和 SNT-8 有显著的诱导凋亡 效应，抗凋亡蛋白 Bcl-xl 以及 JAKs/STATs、MEK/MAPK 信号通路可能参与了这一过程。

 Objective · To identify the effect and potential mechanism of gambogic acid (GA) on natural killer/T-cell lymphoma (NK/TCL) cell lines.  Methods · SNK-1, SNK-6 and SNT-8 were incubated with various concentrations of GA for 24 h, and cell viability was detected with CCK-8 assay. Cell apoptosis was examined by Annexin V-FITC/PI staining assay. Levels of proteins regulating cell apoptosis and phosphorylation levels of proteins in key signaling pathways were detected by Western blotting.  Results · GA showed a potent effect on reduction of cell viability of NK/TCL cell lines in CCK-8 assay. GA increased the percentages of Annexin V positive cells and induced activation of caspase-3 and caspase-9, cleavage of PARP as well as the reduction of Bcl-xl. GA also inhibited the phosphorylation levels of STAT3 in SNK-1 and SNT-8, and ERK1/2 in SNK-1 and SNK-6 significantly.  Conclusion · GA induces cell apoptosis in NK/TCL cell lines SNK-1, SNK-6 and SNT-8. Anti-apoptosis protein Bcl-xl and signaling pathway JAKs/ STATs and MEK/MAPK might be involved in this process.