目的 研究去甲二氢愈创木酸（NDGA）类似物26C的抗肺癌活性与初步机制。方法 利用MTT实验评价26C对肺癌细胞NCI-H460的细胞毒性；用集落克隆、划痕实验分别检测26C对NCI-H460细胞生长、迁移的影响；流式细胞仪检测26C对NCI-H460细胞的周期阻滞及诱导凋亡情况；活性氧簇（ROS）实验探究26C引起细胞凋亡的作用机制。结果 26C对NCI-H460的IC₅₀为（4.7±0.5）μmol/L，对NCI-H460的集落形成、迁移有较强的抑制作用，其活性明显优于先导化合物NDGA；26C可将细胞周期阻滞在G₂/M期，并通过升高ROS水平的作用机制诱导NCI-H460细胞凋亡。结论 化合物26C为具有研发前景的抗肺癌候选化合物，其通过提高ROS水平、阻滞细胞周期来抑制细胞生长和诱导细胞凋亡。

Objective To study the anti-lung cancer activity and preliminary mechanism of NDGA analogue 26C. Methods MTT assay was employed to evaluate the cytotoxicity of 26C to lung cancer cells NCI-H460. Clonogenicity assay and scratch assay were used to investigate the role of 26C on proliferation and migration of NCI-H460 cells, respectively. Flow cytometry detected cycle arrest and apoptosis induction of NCI-H460 cells by 26C, and the intracellular accumulation of ROS was examined to explore the mechanism of 26C inducing apoptosis.Results 26C own an IC₅₀ value of (4.7 ±0.5) μmol/L, and displayed a potent inhibition on clonogenicity and migration in NCI-H460 cells. Additionally, its activity was obviously better than the leading compound NDGA. 26C could arrest the cell cycle in the G₂/M phase and induce apoptosis by accumulating the intracellular ROS. Conclusion With activities of inhibit cell growth and induce apoptosis by increasing ROS levels and arresting the cell cycle, compound 26C could be considered as a potential anti-lung cancer candidate with promising prospects.

浙江省自然科学基金资助项目（LY15H280014）；云南大理药业股份有限公司横向课题（KJHX1603）