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作 者:戴翠萍[1] 张徐宁[1] 薛彩萍[1] 季宁东[1]
机构地区:[1]淮阴卫生高等职业技术学校,淮安市消化道肿瘤重点实验室,江苏淮安223300
出 处:《南京医科大学学报(自然科学版)》2013年第10期1388-1391,共4页Journal of Nanjing Medical University(Natural Sciences)
基 金:江苏省中医药局科技项目(LB09077);淮安市科技支撑计划项目(HAS2009002-2)
摘 要:目的:探讨冰片与顺铂(cisplatin,DDP)联用对耐DDP的食管癌细胞Eca109(DDPr)增殖、细胞周期和凋亡的影响。方法:采用递增药物浓度持续作用诱导法建立耐DDP的食管癌细胞Eca109(DDPr),将冰片联合DDP作用于Eca109(DDPr)细胞,MTT法检测Eca109(DDPr)细胞增殖情况;流式细胞术检测细胞周期及细胞凋亡。结果:递增药物浓度持续作用诱导6个月后,细胞可以在含1μg/ml DDP的培养液中稳定生长,其对DDP的耐药指数为15.886;单用冰片浓度≤1.560μg/ml时,对Eca109(DDPr)细胞无明显抑制作用(P>0.05),但与1μg/ml DDP合用能显著促进DDP对Eca109(DDPr)细胞增殖的抑制作用(P<0.05),并促进DDP诱导Eca109(DDPr)的细胞周期改变、细胞凋亡增加,细胞周期表现为G1期细胞明显增多(P<0.05),S期细胞、G2期细胞明显减少(P<0.05),细胞的凋亡率明显增加(P<0.05)。结论:冰片促进DDP对Eca109(DDPr)细胞增殖的抑制作用,可能与改变Eca109(DDPr)细胞周期、增加细胞凋亡有关。Objective:To explore the effects of borneol combined with cisplatin (DDP) on cell proliferation and cell cycle and apoptosis of human esophageal carcinoma cell line Eca 109 (DDpr). Methods :The human esophageal carcinoma cell line Eca109 was exposed to continuous stepwise-increased concentration of DDP. Drug-sensitivity was measured by MTF. The cell cycle and apoptosis were determined by flow eytometry. Results:After 6 months of stepwise drug exposure, the cell could normally grow and propagate in the medium with 1μg/ml of DDP, and exhibited a resistance index of 15.886 against DDP. The cell line was named Eca109(DDpr). MTT assay showed that borneol at the concentration of no more than 1.560 μg/ml had no obvious inhibition on the growth of Ecal09 (DDPr) cells (P 〉 0.05),but it could significantly promote the inhibition of DDP (1 μg/ml) on the proliferation of Ecal09(DDPr) ceils (P 〈 0.05). Compared with using DDP alone, borneol combined with DDP could change the cell cycle, significantly increase the number of cells in G1 stage (P 〈 0.05) and decrease the number of cells in S stage and G2 stage (P 〈 0.05) ,and obviously promote the apoptosis of Ecal09 (DDPr) cells (P 〈 0.05). Conclusion:Borneol can promote the inhibition of DDP on the proliferation of Ecal09(DDPr) cells,the mechanism may be related to change cell cycle and increase apoptosis of Eca109(DDPr) cells.
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