广西医学

目的分析虎杖苷对人结肠癌SW480细胞迁移和侵袭能力的影响，并基于上皮细胞-间充质转化（EMT)标志物及信号传导与转录激活因子3（STAT3）信号通路探讨其可能的分子机制。方法使用不同浓度（0 μmol/L、25 μmol/L、50 μmol/L、75 μmol/L、100 μmol/L、150 μmol/L）的虎杖苷干预SW480细胞24 h后，采用CCK-8法检测SW480细胞的增殖率，筛选后续实验的干预浓度。使用0 μmol/L、25 μmol/L、50 μmol/L的虎杖苷干预SW480细胞（分别设为0 μmol/L虎杖苷组、25 μmol/L虎杖苷组、50 μmol/L虎杖苷组）24 h后，采用划痕实验、Transwell实验检测SW480细胞迁移和侵袭的能力，采用Western blot检测α-平滑肌肌动蛋白（α-SMA）和波形蛋白的表达水平、磷酸化STAT3（p-STAT3）/STAT3值。结果（1）与0 μmol/L虎杖苷相比，经25 μmol/L、50 μmol/L虎杖苷干预后SW480细胞的增殖率差异无统计学意义（P＞0.05），经75 μmol/L、100 μmol/L、150 μmol/L虎杖苷干预后SW480细胞的增殖率降低（P＜0.05）。与0 μmol/L虎杖苷组相比，25 μmol/L虎杖苷组和50 μmol/L虎杖苷组的划痕愈合率降低（P＜0.05）。Transwell细胞迁移和侵袭实验结果显示，0 μmol/L虎杖苷组、25 μmol/L虎杖苷组、50 μmol/L虎杖苷组的平均穿膜细胞数依次减少（P＜0.05）。与0 μmol/L虎杖苷组相比，50 μmol/L虎杖苷组中α-SMA的表达水平、p-STAT3/STAT3值降低，25 μmol/L虎杖苷组和50 μmol/L虎杖苷组中α-SMA、波形蛋白的表达水平降低（P＜0.05）。结论虎杖苷可能通过抑制STAT3信号通路的活化而逆转EMT，从而发挥抑制SW480细胞迁移和侵袭的作用。

Objective To analyze the effect of polydatin on migration and invasion abilities of human colon cancer SW480 cells, and to explore its possible mechanism based on epithelial-mensenchymal transition (EMT) marker and signal transducer and activator of transcription 3 (STAT3) signaling pathway.MethodsAfter 24 hours of SW480 cells intervention by the application of polydatin in different concentrations (0 μmol/L, 25 μmol/L, 50 μmol/L, 75 μmol/L, 100 μmol/L, and 150 μmol/L), the CCK-8 method was used to detect the proliferation rate of SW480 cells for screening intervention concentration for follow-up experiment. After 24 hours of SW480 cells intervention by employing polydatin of 0 μmol/L, 25 μmol/L, and 50 μmol/L (setting as 0 μmol/L polydatin group, 25 μmol/L polydatin group, and 50 μmol/L polydatin group, respectively), the scratch test and Transwell test were used to detect migration and invasion abilities of SW480 cells. The expressions of α-smooth muscle actin (α-SMA) and vimentin, and phosphorylated STAT3 (p-STAT3)/STAT3 value were detected by using the Western blot. Results(1) Compared with the 0 μmol/L polydatin group, there was no statistically significant difference in the proliferation rate of SW480 cells between post-intervention polydatin of 25 μmol/L and 50 μmol/L (P＞0.05); moreover, the proliferation rate of SW480 cells after intervention by polydatin of 75 μmol/L, 100 μmol/L, and 150 μmol/L were decreased (P＜0.05). Compared with the 0 μmol/L polydatin group, the scratch healing rates of the 25 μmol/L polydatin group and the 50 μmol/L polydatin group were decreased (P＜0.05). The results of Transwell cell migration and invasion tests revealed that average number of transmembrane cells was decreased successively in the 0 μmol/L polydatin group, the 25 μmol/L polydatin group, and the 50 μmol/L polydatin group (P＜0.05). Compared with the 0 μmol/L polydatin group, the expression of α-SMA, and p-STAT3/STAT3 value were decreased in the 50 μmol/L polydatin group, and the expressions of α-SMA and vimentin in the 25 μmol/L polydatin group and the 50 μmol/L polydatin group were decreased (P＜0.05). ConclusionPolydatin may reverse EMT by inhibiting activation of STAT3 signaling pathway, thereby inhibiting effects of migration and invasion of SW480 cells.