白皮杉醇增强顺铂杀伤喉癌Hep-2细胞的作用及其机制

目的 探讨白皮杉醇增强顺铂对喉癌细胞的杀伤作用及其分子机制。方法 体外培养喉癌细胞Hep-2，联合使用白皮杉醇及顺铂，CCK8法检测喉癌Hep-2细胞的增殖能力，流式细胞术检测喉癌Hep-2细胞的凋亡率，Hoechst染色检测喉癌Hep-2细胞中细胞核固缩比例，蛋白印迹法检测BCL-2家族蛋白表达变化。结果 白皮杉醇在50 μmol/L时对喉癌Hep-2细胞的增殖凋亡并无显著影响。与顺铂组相比，白皮杉醇联合顺铂组细胞的增殖能力显著降低，48 h细胞吸光度值白皮杉醇联合顺铂组较顺铂组降低60%，流式细胞术检测发现48 h时，白皮杉醇联合顺铂组喉癌Hep-2细胞的凋亡率显著高于顺铂组（P<0.05），Hoechst染色发现白皮杉醇联合顺铂组喉癌Hep-2细胞的细胞核固缩比例显著增高，差异有统计学意义。蛋白印迹检测发现，白皮杉醇可以显著下调BCL-2蛋白表达水平，上调BAX蛋白表达水平。结论 白皮杉醇可以有效增强顺铂对喉癌细胞的杀伤作用，其分子机制与白皮杉醇可以显著调控BCL-2家族蛋白表达有关。

Mechanism About How Piceatannol Enhances Anti-tumor Effect of Cisplatin on Laryngeal Cancer Hep-2 Cells

Objective To investigate how piceatannol enhances the anti-tumor effect of cisplatin on laryngeal cancer cells and related molecular mechanism. Methods Laryngeal carcinoma Hep-2 cells were cultured in vitro and then treated with piceatannol and cisplatin. Cell proliferation apoptosis, karyopyknosis ratio and proteins expression of BCL-2 family were detected by CCK8, flow cytometry, Hoechst staining and Western blot, respectively. Results No effect of 50 μmol/L piceatannol was found on the Hep-2 cell apoptosis or proliferation. Compared with cisplatin, cisplatin combined with piceatannol could significantly decrease the cell proliferation; after 48h, the absorbance of cells treated with cisplatin and piceatannol was decreased for 60%, and the apoptosis ratio was significantly increased (P<0.05). Hoechst staining revealed the karyopyknosis ratio of Hep-2 cells treated with cisplatin and piceatannol was significantly increased. Western blot showed piceatannol could down-regulate BCL-2 expression and up-regulate BAX expression. Conclusion The anti-tumor effect of cisplatin on laryngeal cancer cells could be enhanced by piceatannol, and its molecular mechanism is related to the regulatory effect of piceatannol on the key proteins of BCL-2 family.