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目的研究沙利度胺联合FOLFOX(folinic acid fluorouracil oxaliplatin)作用肝癌细胞HepG2后VEGF、Caspase-3的表达,以及探讨沙利度胺联合FOLFOX诱导HepG2细胞凋亡的机制。方法应用MTT法和流式细胞仪体外研究沙利度胺对HepG2细胞增殖的影响;采用western blot法,观察沙利度胺联合FOLFOX作用HepG2细胞48h后VEGF、Caspase-3的表达情况。结果沙利度胺对肝癌HepG2细胞有抑制作用,且沙利度胺联合FOLFOX显著提高了对肝癌细胞生长的抑制作用,沙利度胺联合FOLFOX作用于HepG2细胞48h后,细胞表面Caspase-3的表达均增强,VEGF的表达均降低。结论沙利度胺联合FOLFOX诱导肝癌HepG2细胞凋亡的机制可能可能通过调节VEGF蛋白表达激活caspase-3,从而诱导HepG2细胞凋亡。
Objective To study the expression of VEGF and Caspase-3 in HepG2 cells treated with FOLFOX combined with folinic acid fluorouracil oxaliplatin, and to explore the mechanism of thalidomide combined with FOLFOX in inducing HepG2 cells apoptosis. Methods The effects of thalidomide on the proliferation of HepG2 cells were studied by MTT assay and flow cytometry. The expressions of VEGF and Caspase-3 in HepG2 cells treated with thalidomide and FOLFOX were observed by western blot. Results Thalidomide had inhibitory effect on HepG2 cells, and thalidomide combined with FOLFOX significantly inhibited the growth of HepG2 cells. After thalidomide combined with FOLFOX for 48 h, the expression of Caspase-3 The expression of VEGF was increased and the expression of VEGF was decreased. Conclusion The mechanism of thalidomide combined with FOLFOX in inducing HepG2 cell apoptosis may induce apoptosis of HepG2 cells by regulating the expression of VEGF protein and activating caspase-3.