目的：观察红景天苷对宫颈鳞癌C33A细胞增殖、侵袭及凋亡的影响并初步探讨其可能的机制。方法：将C33A细胞分为4 组：对照组、低剂量组（红景天苷50 μg/ml）、高剂量组（红景天苷150 μg/ml）、抑制剂AG490 组（JAK2/STAT3 信号通路抑制剂AG490 50 μmol/L），采用MTT 法、EdU 标记实验、Transwell 实验、Rh123 染色和流式细胞术分别检测红景天苷和AG490 对C33A 细胞增殖、侵袭和凋亡的影响，Western blotting 检测红景天苷和AG490 对C33A 细胞中JAK2/STAT3 通路相关蛋白（p-JAK2、p-STAT3）和凋亡相关蛋白（Bax、Bcl-2、caspase-3）表达的影响。结果：与对照组相比，低剂量组C33A细胞的增殖和DNA的合成明显受到抑制（均P<0.05）、侵袭能力明显降低（均P<0.05）、Rh123 荧光强度明显减弱（均P<0.05）、线粒体膜结构受到破坏、细胞凋亡率明显增加（均P<0.05）；p-JAK2、p-STAT3、Bcl-2 水平显著下降（均P<0.05）、Bax、caspase-3 的表达水平显著升高（P<0.05）；与低剂量组相比，高剂量组、抑制剂组对C33A细胞增殖、侵袭、凋亡及相关蛋白表达的影响更为显著（P<0.05）；而高剂量组、抑制剂组间无显著差异。结论：红景天苷可以抑制C33A细胞的增殖和侵袭、促进细胞凋亡，其作用机制可能与抑制JAK2/STAT3 信号通路有关。

Objective: To investigate the effects of salidroside on the proliferation, invasion and apoptosis of cervical squamous cell carcinoma C33A cells and explore its possible mechanism. Methods: C33A cells were divided into 4 groups: control group, low-dose group (salidroside 50 μg/mL), high-dose group (salidroside 150 μg/mL), and AG490 group (inhibitor of JAK2/STAT3 signaling pathway,50 μmol/L). Effects of salidroside and AG490 on the proliferation, invasion and apoptosis of C33A cells were detected by MTT method, EdU labeling experiment, Transwell assay, Rh123 staining and Flow cytometry, respectively. Western blotting was used to detect the effects of salidroside and AG490 on the expressions of JAK2/STAT3 pathway-related proteins (p-JAK2, p-STAT3) and apoptosis-related proteins (Bax, Bcl-2, caspase-3) in C33A cells. Result: Compared with the control group, the proliferation and DNA synthesis as well as the invasion of C33A cells in the low-dose group were significantly inhibited (all P<0.05), while the apoptosis was significantly enhanced (P<0.05); in the meanwhile, the fluorescence intensity of Rh123 was significantly reduced (all P<0.05) and the membrane structure of C33A cells were destroyed; moreover, the expressions of p-JAK2, p-STAT3 and Bcl-2 were significantly decreased while the expressions of Bax and caspase-3 were significantly increased (all P<0.05). Compared with the low-dose group, the effects of high-dose salidroside and AG490 on the proliferation, invasion, apoptosis and related protein expressions in C33A cells were more significant (all P<0.05), but there was no difference between the high-dose group and the AG490 group. Conclusion: Salidroside can inhibit the proliferation and invasion of C33A cells and promote cell apoptosis. Its mechanism may be related to inhibition of JAK2/STAT3 signaling pathway.