丹皮酚对食管癌细胞放射增敏作用及其机制

目的通过研究丹皮酚对食管鳞癌细胞株KYSE450、TE10放射敏感性的影响及探讨该作用的分子机制，为丹皮酚作为放射治疗增敏药物应用于食管鳞癌的综合治疗提供根据。方法稳定培养食管癌细胞株，经不同浓度的丹皮酚作用后，CCK8法检测细胞增殖。克隆形成实验检测细胞克隆形成能力，流式细胞术（FCM）检测细胞凋亡相关蛋白的表达。Western blotting实验检测凋亡相关蛋白的表达情况。结果丹皮酚剂量依赖性地抑制食管癌细胞的增殖（P < 0.05~P < 0.01），并且抑制放射治疗后的肿瘤细胞克隆形成能力，增加肿瘤细胞的凋亡率（P < 0.01）；Western blotting实验表示放疗与丹皮酚联合处理可降低Bcl-2的表达，增加Bax、caspase-3、cleaved caspase-3、PARP的表达。结论丹皮酚联合放疗可通过下调Bcl-2表达，上调Bax、caspase-3、PARP、cleaved caspase-3表达，从而抑制体外食管癌细胞的生长，实现放疗增敏。

Effect of paeonol on the radiosensitization of esophageal cancer celland its mechanism

ObjectiveTo study the effects of paeonol on the radiosensitivity of esophageal squamous carcinoma cell lines KYSE450 and TE10, explore its molecular mechanism, and provide a new basis for the comprehensive treatment of esophageal squamous cell carcinoma with paeonol as radiotherapy sensitizing drug.MethodsEsophageal cancer cell lines were stably cultured.After the cells were treated with different concentrations of paeonol, the CCK8 method was used to detect the proliferation of cells, the ability of colony formation was detected using colony formation assay, the apoptosis was detected using flow cytometry, and the expression of apoptosis-related protein was detected using Western blotting.ResultsPaeonol could inhibit the proliferation of esophageal cancer cells at a concentration-dependent manner, inhibit the colony-forming ability of tumor cells after radiotherapy, and increase the apoptosis rate of tumor cells.The results of Western blotting analysis showed that the radiotherapy combined with paeonol could reduce the expression of Bcl-2, and increase the expression levels of Bax, caspase-3, cleaved caspase-3 and PARP.ConclusionsPaeonol combined with radiation therapy can inhibit the expression of Bcl-2, up-regulate the expression levels of Bax, caspase-3, cleaved caspase-3 and PARP, and the growth of esophageal cancer cells in vitro is inhibited to improve the radiosensitization.