为探究11-羰基-β-乙酰乳香酸（acetyl-11-keto-β-boswellic acid，AKBA）对皮肤T细胞淋巴瘤（cutaneous T cell lymphoma，CTCL）细胞系HuT 78增殖和凋亡的影响及作用机制，用不同浓度的AKBA处理HuT 78细胞系24、48 h后，应用CCK-8法检测HuT 78细胞的增殖；应用FACS检测肿瘤细胞的凋亡水平；通过Real-time PCR及Western blotting检测凋亡相关基因及蛋白的表达水平。结果显示，AKBA通过抑制HuT 78细胞NF-κB抑制蛋白α（NF-κB inhibitor alpha，IκB-α）的磷酸化抑制NF-κB活化；下调抗凋亡蛋白Bcl-xL、Bcl-2的表达，促进caspase3的活化降解，同时上调Fas的配体FasL的表达，对HuT 78细胞发挥抑制增殖和促进凋亡的作用，可作为免疫治疗的候选药物。

This study aims to investigate the anti-tumor effects of acetyl-11-keto-β-boswellic acid (AKBA) on cutaneous T cell lymphoma (CTCL) cell line HuT 78, and to explore the underlying mechanisms. After AKBA treatments of different concentrations for 24 and 48 hours, the cell proliferation of HuT 78 cells was measured by CCK-8 assay and the apoptosis induced by AKBA was detected by FACS using Annexin Ⅴ/PI staining. The apoptosis-related genes and proteins levels were analyzed by Real-time PCR and Western blotting, respectively. The results showed that AKBA inhibited the proliferation of HuT 78 cells and induced apoptosis through down-regulating NF-κB pathway via inhibiting phosphorylation of NF-κB inhibitor alpha (IκB-α). In the meantime, AKBA down-regulated the anti-apoptosis proteins Bcl-xL and Bcl-2, induced degradation of caspase3 and up-regulated the expression of FasL. In summary, AKBA is a candidate compound for the treatment of CTCL.