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目的观察金莲花中提取的牡荆苷体外对人食管癌EC-109细胞生长及诱导EC-109细胞凋亡的作用,探讨p53及bcl-2蛋白表达在牡荆苷抗肿瘤细胞机制中的作用。方法用不同浓度牡荆苷作用于对数生长期的EC-109细胞,通过CCK-8法检测其对EC-109细胞体外生长、增殖的抑制作用;Hoechst33258荧光染色观察细胞形态的变化;琼脂糖凝胶电泳检测DNA条带;AnnexinV-FITC/PI双标法流式细胞术观察牡荆苷对EC-109细胞凋亡的诱导作用;流式细胞术检测EC-109细胞中抑癌基因p53和促癌基因bcl-2蛋白的表达。结果牡荆苷对EC-109细胞生长、增殖具有明显的抑制作用,能够诱导EC-109细胞凋亡,且作用与牡荆苷浓度、作用时间呈正相关,可上调p53蛋白表达,下调bcl-2蛋白表达。结论牡荆苷可能通过上调p53蛋白和下调bcl-2蛋白的表达,促进EC-109细胞凋亡,抑制EC-109细胞生长。
Objective To observe the effect of vitexin extracted from Trollius chinensis on the growth of human esophageal carcinoma EC-109 cells and the induction of EC-109 cell apoptosis in vitro and to explore the role of p53 and bcl-2 protein expression in anti-tumor cell mechanism of vitexin . Methods EC-109 cells were treated with different concentrations of vitexin in vitro and the inhibitory effects on the growth and proliferation of EC-109 cells were detected by CCK-8 assay. The morphological changes were observed by Hoechst 33258 staining. Sepharose The DNA bands were detected by gel electrophoresis. Annexin V-FITC / PI double-labeled flow cytometry was used to observe the induction effect of vitexin on EC-109 cells. The expression of p53 and The expression of oncogene bcl-2 protein. Results Vitexin significantly inhibited the growth and proliferation of EC-109 cells and induced the apoptosis of EC-109 cells. The results showed that vitexin had a positive correlation with vitexin concentration and action time, and up-regulated the expression of p53 protein and decreased the expression of bcl-2 Protein. Conclusion Vitexin may promote the apoptosis of EC-109 cells and inhibit the growth of EC-109 cells by up-regulating p53 protein and down-regulating bcl-2 protein expression.