中文摘要：

目的初步探讨α／β干扰素抑制淋巴瘤细胞增殖的分子机制。方法用IFN-α／β处理淋巴瘤细胞（Namalwa、JeKo-1）和白血病细胞（Jurkat、THP-1）24h，CCK-8法检测IFN-α／β对上述细胞的增殖抑制效果；RT-PCR、realtimePCR、Westernblot检测其SARImRNA和蛋白水平的变化；对SARI基因启动子区的转录因子结合位点进行生物信息学预测。结果IFN-α和IFN-β均可有效杀伤Namalwa和JeKo-1淋巴瘤细胞（P〈0．05），且均能显著诱导淋巴瘤细胞SARImRNA和蛋白的表达（P〈0．05），但两种干扰素对Jurkat和THP-1白血病细胞的存活及SARI的表达均无显著影响（P〉0．05）；生物信息学分析显示，SARI启动子区含有转录因子STAT的结合位点。结论上调SARI表达可能是IFN-α／β抑制淋巴瘤细胞增殖的机制之一，而SARI的上调可能是由STAT介导的。

英文摘要：

Objective To investigate the mechanism of interferon-α/β （IFN-α/β） inhibiting lymphoma cell proliferation. Methods Lymphoma cells （Namalwa and JeKo-1 ） and leukemia cells （Jurkat and THP-1 ） were treated with IFN-α/β for 24 h. Cell viability was measured by CCK-8 assay. The mRNA and protein expression levels of SARI were detected by reverse transcription PCR, real-time PCR and Western blotting. The transcription factor binding sites in SARI gene promoter region were predicted using bioinformatics method. Results Lymphoma cells （Namalwa and JeKo-1 ） were effectively killed by both IFN-α and IFN-β （ P 〈 0. 05 ）, and the mRNA and protein expression levels of SARI were significantly up-regulated （ P 〈 0.05 ）. However, IFN-α/β had no significant effect on cell viability and SARI expression of leukemia cells （Jurkat and THP-1 ） （P 〉 0.05 ）. Bioinformatics results revealed that transcription factor STAT might bind to SARI gene promoter region. Conclusion Upregulation of SARI, which is possibly mediated by STAT, may be involved in the process of IFN-α/β inhibiting lymphoma cell proliferation.