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Effect of solanine on the membrane potential of mitochondria in HepG_2 cells and [Ca^(2+)]i in the cells 被引量:17
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作者 Shi-Yong Gao Qiu-Juan Wang Yu-Bin Ji 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第21期3359-3367,共9页
AIM: To observe the effect of solanine on the membrane potential of mitochondria in HepG2 cells and [Ca^2+]i in the cells, and to uncover the mechanism by which solanine induces apoptosis.METHODS: HepG2 cells were ... AIM: To observe the effect of solanine on the membrane potential of mitochondria in HepG2 cells and [Ca^2+]i in the cells, and to uncover the mechanism by which solanine induces apoptosis.METHODS: HepG2 cells were double stained with AO/EB, and morphological changes of the cells were observed using laser confocal scanning microscopy (LCSM). HepG2 cells were stained with TMRE, and change in the membrane potential of mitochondria in the cells were observed using LCSM. HepG2 cells were double stained with Fluo-3/AM, and change of [Ca^2+]i in the cells were observed using LCSM. HepG2 cells were double stained with TMRE and Fluo-3/AM, and both the change in membrane potential of mitochondria and that of [Ca^2+]i in the cells were observed using LCSM.RESULTS: Cells in treated groups showed typical signs of apoptosis. Staining with TMRE showed that solanine could lower membrane potential; staining with Fluo-3/AM showed that solanine could increase the concentration of Ca^2+ in tumor cells; and those of double staining with TMRE and Fluo-3/AM showed that solanine could increase the concentration of Ca^2+ in the cells at the same time as it lowered the membrane potential of mitochondria.CONCLUSION: Solanine opens up the PT channels in the membrane by lowering the membrane potential, leading to Ca^2+ being transported down its concentration gradient, which in turn leads to the rise of the concentration of Ca^2+ in the cell, turning on the mechanism for apoptosis. 展开更多
关键词 SOLANINE hepatocarcinomatic cell Ca^2+ in the cell Membrane potential Laser confocal scanning microscopy
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细胞外调节蛋白激酶与端粒酶对肝癌和白血病细胞系凋亡的调控作用(英文) 被引量:2
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作者 李登举 张瑶珍 +2 位作者 孟凡凯 张东华 刘文励 《中国实验血液学杂志》 CAS CSCD 2002年第4期294-298,共5页
为了观察化疗药物三尖杉酯碱(HRT)、长春新碱(VCR)和依托泊苷(VP-16)抑制肝癌细胞系SMMC7721和白血病细胞系K562细胞增殖、促进细胞凋亡过程中端粒酶活性及细胞外调节蛋白激酶(ERK)磷酸化蛋白表达水平的变化,应用MTT、流式细胞术、端粒... 为了观察化疗药物三尖杉酯碱(HRT)、长春新碱(VCR)和依托泊苷(VP-16)抑制肝癌细胞系SMMC7721和白血病细胞系K562细胞增殖、促进细胞凋亡过程中端粒酶活性及细胞外调节蛋白激酶(ERK)磷酸化蛋白表达水平的变化,应用MTT、流式细胞术、端粒重复序列扩增法(TRAP)、生物发光分析及Western印迹等方法进行了检测和分析。研究结果发现,一定浓度的化疗药物作用24小时后,可以抑制细胞增殖、诱导细胞凋亡;在同样作用条件下,端粒酶活性和磷酸化ERK1/2的表达也受到一定程度的抑制,其中以HRT的作用最明显。结论:HRT,VCR和VP-16可能是通过抑制Ras/Raf/MEK/ERK1/2信号传导通路、降低ERK活性、减少ERK1/2靶基因的转录活化、间接下调端粒酶活性这一共同的作用机制而发挥作用的;细胞凋亡是端粒持续缺失的的结果。 展开更多
关键词 肝癌 白血病 细胞外调节蛋白激酶 端粒酶 肝癌细胞系 白血病细胞系 细胞凋亡 三尖杉酯碱 长春新碱 依托泊苷
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