目的：探讨阿曼托双黄酮（AF）对甲状腺癌SW579 细胞中 JAK2-STAT3 通路活化及其细胞增殖和凋亡的影响。方法：用0、50、100、150、200 μmol/L 的AF处理SW579 细胞24、48、72 h，采用CCK-8和Celigo 计数、FCM、WB及qPCR法检测AF对SW579 细胞的增殖、凋亡、JAK2-STAT3 通路活化及其下游调控基因c-Myc、Bcl2、survivin 的mRNA 及蛋白表达水平的影响。结果：AF 处理后，SW579 细胞增殖能力显著下降（P<0.05）且呈浓度依赖性，细胞凋亡呈浓度依赖性增多（P<0.05），细胞中JAK2-STAT3通路的活化受到显著抑制（P<0.05），其下游基因c-Myc、Bcl2、survivin 的mRNA及蛋白表达均明显下降（均P<0.05）。结论：AF 可通过抑制SW579 细胞中JAK2-STAT3通路活化及其下游基因的表达而抑制SW579 细胞的增殖并促进其凋亡，有望成为治疗甲状腺癌的有效药物。

Objective: To investigate the effects of Amentoflavone (AF) on the JAK2-STAT3 pathway activation, apoptosis，and proliferation of thyroid carcinoma SW579 cells. Methods: SW579 cells were treated with AF at different concentrations (0，50, 100, 150, and 200 μmol/L) for 24 h, 48 h, and 72 h, respectively. Then, the effects of AF on the proliferation and apoptosis of SW579 cells were detected by CCK-8 and Celigo cell count and FCM, respectively; and the effects of AF on the JAK2-STAT3 pathway activation and the mRNA and protein expression of its downstream genes c-Myc, Bcl2 and Survivin in SW579 cells were detected by qPCR and Western blotting. Results: After the treatment with AF, the proliferation of SW579 cells was suppressed significantly while the apoptosis was promoted significantly, which were all in a dose-dependent manner (both P<0.05). The activation of JAK2-STAT3 pathway was significantly inhibited (P<0.05), and the mRNA and protein expression of the downstream genes c-Myc, Bcl2, and survivin in SW579 cells was significantly decreased (all P<0.05) after the treatment with AF. Conclusion: AF may contribute to apoptosis induction and proliferation suppression of thyroid carcinoma SW579 cells via inhibiting the activation of JAK2-STAT3 pathway and its downstream gene expression. AF has the potential to serve as a novel therapeutic approach for the management of thyroid carcinoma.

国家自然科学基金（No. 81602327）