雷公藤红素对非小细胞肺癌细胞株H1299增殖与凋亡的影响

目的：研究雷公藤红素对非小细胞肺癌细胞株H1299的杀伤作用及相关调控机制。方法：用细胞计数法测定不同浓度雷公藤红素对H1299细胞增殖的影响;用流式细胞仪检测H1299细胞的细胞周期;用Western blotting检测剪切的（cleaved）聚ADP核糖聚合酶（PARP）、cleaved caspase-3和低氧诱导因子-1（HIF-1）的表达水平;用DCF-DA染色和荧光显微镜检测细胞内的活性氧（ROS）水平;用萤光素酶活性测定法检测NFκB的活性。结果：雷公藤红素以时间和剂量依赖性的方式抑制H1299细胞的增殖,并使细胞阻滞在G2/M期。同时,雷公藤红素显著上调cleaved PARP和cleaved caspase-3的表达,提高细胞内的ROS水平,并且抑制NFκB的活性。结论：雷公藤红素以时间和剂量依赖性的方式抑制H1299细胞的增殖,并诱导caspase依赖性的细胞凋亡,具体机制与细胞内ROS的积累和NFκB的活性抑制有关。

Role of Celastrol in Regulating Proliferation and Apoptosis of Non-Small Cell Lung Cancer H1299 Cells

Objective： To investigate the role and regulating mechanism of celastrol in killing non-small cell lung cancer H1299 cells. Methods： The proliferation inhibition of H1299 cells induced by celastrol was measured by cell counting. Cell cycle of H1299 cells was analyzed by flow cytometry. Western blotting was used to determine the expression of cleaved PARP, cleaved easpase-3 and HIF-1. The level of reactive oxygen species（ROS） was detected by DCF-DA stain- ing and fluorescence microscopy. The activity of NFKB was determined by luciferase assay. Results： Celastrol induced time and dose-dependent growth arrest of H1299 cells and blocked cell cycle into G2/M phase. Moreover, celastrol upregulated the expression of cleaved PARP and cleaved caspase-3, induced ROS accumulation and inhibited the activity of NFKB. Conclusion： Celastrol induces time and dose-dependent growth arrest and caspase-dependent apoptosis in H1299 cells, which was associated with ROS accumulation and inhibition of NFKB.