紫花牡荆素诱导食管癌细胞凋亡的分子机制

Molecular mechanism of Casticin to induce apoptosis on esophagus carcinoma cells

目的观察紫花牡荆素对食管癌(esophagus carcinoma,EC)细胞增殖能力的影响并探讨其分子机制。方法以噻唑蓝比色法与侵袭实验检测不同浓度紫花牡荆素处理对食管癌细胞株EC9706与EC109细胞增殖能力的影响,流式细胞术定量分析细胞凋亡率,Western blotting检测凋亡相关蛋白B淋巴细胞瘤-2相关蛋白(B-cell lymphoma-2 associated X protein,BAX)、活化型Caspase-3及血管内皮生长因子(vascular endo-thelial growth factor,VEGF)表达变化。结果不同浓度紫花牡荆素处理显著抑制EC9706与EC109细胞增殖水平并诱导细胞凋亡,同未加药(0μmol/L)组比较差异均有统计学意义(P<0.05);紫花牡荆素处理可以上调BAX与Caspase-3表达水平,下调VEGF表达水平。结论紫花牡荆素处理后导致BAX和活化型Caspase-3表达上调、VEGF表达下调可能是其抑制食管癌细胞增殖并诱导细胞凋亡的重要分子机制。

ObjectiveTo investigate the effects of casticin on proliferation of esophagus carcinoma cells. MethodsThiazolyl blue tetrazolium bromide （MTT） assay and Annexin Ⅴ propidium iodinate （PI） staining assays were performed to observe the inhibitory effect of casticin and the rate of apoptosis on EC9706 and EC109 cells respectively. The expression of B cell lymphoma 2 associated X protein （BAX）, Caspase3 and vascular endothelial growth factor （VEGF） was analyzed by Western blot.ResultsExposure to casticin significantly presented functions of growth suppression and apoptosis inducton on EC9706 and EC109 cells in a dose dependent manner （P〈005）. Additionally, BAX and Caspase 3 expression were increased after treatment with casticin, whereas VEGF expression was down regulated. ConclusionCasticin possesses a significant function to inhibit proliferation and induce apoptosis on esophagus carcinoma cells, which may be due to the increased BAX and Caspase 3 expression as well as suppressed VEGF expression.