目的 探究七氟醚对卵巢癌细胞SKOV3干细胞特性及增殖、侵袭迁移能力的影响。方法 常规培养人卵巢癌细胞SKOV3于培养瓶中，分为七氟醚组及对照组，七氟醚组以5% CO₂和1%七氟醚培养24 h，对照组仅以5% CO₂培养24 h，MTT法检测两组细胞增殖能力的变化，Transwell侵袭及迁移实验检测细胞侵袭及迁移能力，Western blotting检测两组细胞干细胞特性相关分子（Oct4及Sox2）及上皮间充质转化（EMT）相关分子（E-cadherin、Vimentin）的表达差异。结果 七氟醚组细胞72、96 h时间点增殖能力显著低于对照组，差异具有统计学意义（P<0.05）。七氟醚组穿透Matrigel基质胶的细胞数、迁出Transwell上小室的细胞数均明显少于对照组，差异具有统计学意义（P<0.05）。七氟醚组Oct4、Sox2、Vimentin表达均显著低于对照组，E-cadherin表达显著高于对照组，差异具有统计学意义（P<0.05）。结论 七氟醚可通过减轻卵巢癌细胞EMT进程及干细胞特性，抑制细胞增殖及侵袭迁移能力。

Objective To investigate the effects of sevoflurane on the characteristics of stem cells, proliferation, invasion and migration ability of ovarian cancer cell SKOV3. Methods Human ovarian cancer cells SKOV3 in culture flask were divided into sevoflurane and control group. The sevoflurane group cell was cultured under environment of 5%CO₂ and 1% sevoflurane for 24 h, and the control group cell was cultured under environment of 5%CO₂ for 24 h. MTT method was used to detect the ability of cell proliferation of two groups of cell. Transwell invasion and migration assay were used to detect the ability of cell invasion and migration of two groups of cell. Western blotting was used to detect the expression of stem cell related molecular (Oct4 and Sox2) and epithelial mesenchymal transition (EMT) related molecules (E-cadherin, Vimentin). Results The proliferation ability of the sevoflurane group was significantly lower than that of the control group at 72 and 96 h, and the difference was statistically significant (P<0.05). The number of sevoflurane cells through the matrigel and transwell chamber were less than control group, the difference was statistically significant (P<0.05). The expression of molecular stem cell related Oct4 and Sox2 in sevoflurane group were lower than that in control group, the difference was statistically significant (P<0.05). The expression of molecular EMT related E-cadherin and Vimentin were lower than that in control group, the difference was statistically significant (P<0.05). Conclusion Sevoflurane can inhibit the ability of proliferation, invasion and migration in ovarian cancer cells by reducing the EMT process and stem cell characteristics.