目的：观察紫草素对人食管癌TE-1细胞增殖、凋亡和细胞周期的影响，并探究其作用机制。方法：采用不同浓度的 紫草素（0、 1、 5、 10 μmol/L）处理TE-1细胞，MTT法检测24、 48、 72 h后各组细胞增殖水平；紫草素处理各组TE-1细胞48 h后，采用 Hoechst 33258荧光染色观察细胞凋亡状况，流式细胞术检测细胞的凋亡水平及周期变化，Western blotting检测TRAP1/Akt/ mTOR信号通路相关蛋白表达变化。结果：紫草素呈时间和浓度依赖性抑制TE-1细胞增殖（P<0.05或P<0.01）；与对照组相比， 紫草素能显著促进TE-1细胞凋亡（P<0.01）， 使TE-1细胞周期发生G0/G1期阻滞（P<0.05或P<0.01），同时降低TRAP1、p-Akt以及 p-mTOR表达水平（P<0.05或P<0.01），以上作用具有剂量依赖性。结论：紫草素能显著抑制TE-1细胞的增殖，诱导细胞发生G0/ G1期阻滞并促进其凋亡，这可能与其抑制TRAP1/Akt/mTOR信号通路有关。

Objective: To observe the effects of shikonin on the proliferation, apoptosis and cell cycle of human esophageal carcinoma TE-1 cells, and to explore its mechanism. Methods: TE-1 cells were treated with different concentrations of shikonin (0, 1, 5, 10 μmol/L). MTT assay was used to detect cell proliferation at different time points (24, 48 and 72 h). After treatment with shikonin for 48 h, cell apoptosis in TE-1 cells of each group was observed with Hoechst 33258 fluorescence staining. Flow cytometry was used to detect apoptosis and cell cycle. The changes in expression of TRAP1/Akt/mTOR signaling pathway related proteins were detected by Western blotting. Results: Shikonin inhibited the proliferation of TE-1 cells in a time-dose-dependent manner (P<0.05 or P<0.01). Compared with the control group, shikonin significantly promoted the apoptosis of TE-1 cells (P<0.01), induced the G0/G1 phase block of TE-1 cells (P<0.05 or P<0.01), and reduced the expression levels of TRAP1, p-Akt and p-MTOR (P<0.05 or P<0.01). The above effects were all dose-dependent. Conclusion: Shikonin can significantly inhibit the proliferation of TE-1 cells in vitro, induce G0/G1 phase arrest and promote apoptosis, which may be closely related to the inhibition of TRAP1/Akt/mTOR signaling pathway.