中文摘要：

目的：探讨曲古菌素A（TSA）联合全反式维甲酸（ATRA）诱导宫颈癌SiHa细胞凋亡的协同作用及其相关机制。方法：TSA与ATRA联合或者单独作用于SiHa细胞,采用CellTiter 96Aqueous法检测细胞增殖情况,7AAD荧光染色法观察细胞凋亡形态,Annexin V/7AAD法流式细胞术检测细胞凋亡率,Western Blot法检测P53、BCL-2和Caspase-3蛋白的表达变化。结果：细胞增殖实验结果显示TSA联合ATRA对SiHa细胞有显著的增殖抑制作用;7AAD荧光染色结果显示联合用药组细胞凋亡明显增加,出现核碎裂等典型凋亡改变;流式细胞术检测结果显示联合用药组凋亡率显著增高;Western Blot结果显示：与对照组比较,联合用药组中P53和活化性Caspase-3蛋白的表达水平显著升高,而BCL-2蛋白表达水平显著下降。结论：TSA联合ATRA在体外对SiHa细胞具有明显的协同抑制增殖和诱导凋亡作用,推测其机制可能与P53和活化性Caspase-3蛋白表达水平上调、BCL-2蛋白表达水平下调有关。

英文摘要：

Objective： To explore the synergistic effect of trichostatina A combined with all - trans retinoic acid on induction of ap- optosis of cervical cancer SiHa cells and the relevant mechanism. Methods： SiHa cells were treated with combined TSA and ATRA or single TSA or single ATRA, CellTiter 96 Aqueous method was used to detect proliferation of SiHa cells, 7AAD fluorescent staining was used to observe the morphology of cell apoptosis, Annexin/TAAD flow cytometry were used to detect the rate of cell apoptosis, Western Blot was used to detect the changes of expressions of P53, BCL - 2, and Caspase - 3. Results： The results of cell proliferative test showed that TSA com- bined with ATRA can inhibit SiHa cells significantly; the results of 7AAD fluorescent staining showed that the apoptosis of cells in combined therapy group increased obviously, typical apoptotic manifestations such as nuclear fragmentation appeared; the results of flow cytometry showed that the rate of apoptosis in combined therapy group increased significantly; the results of Western Blot showed that the expression levels of P53 protein and activated Caspase -3 protein in combined therapy group increased significantly, while the expression level of BCL - 2 protein decreased significantly. Conclusion： TSA combined with ATRA had synergistic effect on proliferation inhibition and induction of apoptosis for SiHa cells in vitro significantly, it is supposed that the mechanism may be related to up - regulations of P53 protein and activa- ted Caspase - 3 protein protein, down - regulation of BCL - 2 protein.