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作 者:胡硕[1] 胡成平[1] 梁昌华[1] 黄柏英[2]
机构地区:[1]中南大学湘雅医院,湖南长沙410008 [2]中南大学细胞培养中心,湖南长沙410008
出 处:《湖南中医学院学报》2005年第2期14-16,共3页Journal of Hunan College of Traditional Chinese Medicine
基 金:湖南省科技厅科研基金课题 (0 3SSY3 0 5 4)
摘 要:目的探讨人参单体Rh2对肺腺癌耐药A5 49DDP细胞的促凋亡作用。方法用MTT法分别检测顺铂和Rh2对A5 49细胞、A5 49DDP细胞的抑制率(IC)。将Rh2作用于A5 49DDP细胞,Hoechst3 3 2 5 8染色荧光显微镜下观察细胞核形态,流式细胞仪检测细胞跨膜电位(Δψ)。结果顺铂对A5 49细胞、A5 49DDP细胞的IC50 分别为2 4 μmol/L、32 5 μmol/L ,耐药指数为13.5 4。Rh2 >10 μmol/L时,对A5 4 9DDP细胞有明显抑制作用,且与Rh2的浓度有一定的依赖关系。Rh2作用后A5 4 9DDP细胞核缩小或变形,荧光成团块分布,有凋亡小体形成;细胞线粒体跨膜电位显著性降低(P <0 .0 1)。结论Rh2能促使A5 4 9DDP细胞凋亡,其可能是通过降低细胞的线粒体跨膜电位来诱导细胞凋亡。Objective To explore the effects of Gensenoside Rh2 on lung adenocarcinoma cells.Methods The method of MTT was applied to test the resistance of cisplatin and Gensenoside Rh2 to A549 cells and A549DDP cells respectively. Cellular morphology was observed under fluorescence microscope. Membrane potential of mitochondrion (Δψ) was inspected with flow cytometry. Results IC 50 of cisplatine to A549 cells and to A549DDP cells were 24?μmol?/L and 325?μmol?/L respectively. When Rh2>10?μmol?/L,A549 cells and A549DDP cells were restrained obviously. Observed under fluorescence microscope, fluorescence was distributed uniformly on A549DD cell nucleus without treatment.After treated by Rh2, fluorescence was conglomerated like grain on the cell nucleus.Many cell nucleus were shrunk or distorted. Δψ of cells treated by Rh2 were markedly lower than that without treatment, P<0.01. Conclusions Gensenoside Rh2 can cause A549DDP cells apoptosis by reducing Δψ of cells.
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