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Effect of Asparagus saponins on HepG2 Apoptosis and mitochondrial membrane potential and ROS Level

机译:芦笋皂苷对HepG2细胞凋亡和线粒体膜电位和ROS水平的影响

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To study the effect of Saponins of asparagus on HepG2 apoptosis, reactive oxygen species (ROS) and mitochondrial membrane potential (Δψm) levels. Saponins of asparagus with different concentration was treated with HepG2 at different time, MTT assay was used to detect inhibitory rate, fluorescence staining was used to observe apoptosis morphology, flow cytometry was used to detect apoptosis rate and cell cycle, also ROS and Δψm were measured by flow cytometry. Results showed Saponins of asparagus inhibited cell proliferation; the IC50 on HepG2 was 172.3 μg/mL. Apoptosis morphology was observed by fluorescence microscope, some of the cells had changed from irregular shapes into round cells, the nuclei had decreased in size, the number of nucleoli had decreased; the chromatin had condensed, with the cytoplasm becoming more concentrated. The cell cycle of HepG2 was arrested at S phase, G2/M phase percent decreased. After 72h the treated group appeared apoptosis peak, and apoptosis rate with high dose group 30.94±1.74%; After 48h the ROS in treated group increased with high dose group 77.7±4.5%; and Δψm decreased with high dose group 77.8±1.9% From the above it can be seen that Asparagus saponins have a relatively strong inhibitory effect on HepG2 cells, and the mechanism involved has to do with their role in increasing the production of intracellular ROS, which leads to the lowering of mitochondrial membrane potential, thus initiating the apoptosis mechanism that induces apoptosis in HepG2 cells.
机译:为了研究芦笋皂苷对HepG2细胞凋亡,反应性氧物质(ROS)和线粒体膜电位(Δψm)水平的影响。在不同时间用Hepg2处理芦笋的皂苷,使用MTT测定来检测抑制率,使用荧光染色来观察细胞凋亡的形貌,流式细胞术用于检测细胞凋亡率和细胞周期,还测量ROS和ΔψM通过流式细胞术。结果显示芦笋皂苷抑制细胞增殖; HepG2上的IC 50为172.3μg/ ml。通过荧光显微镜观察细胞凋亡形态,一些细胞从不规则形状变为圆形细胞,核的尺寸下降,核仁的数量降低;染色质浓缩,细胞质变得更浓缩。 HepG2的细胞周期在S期被捕,G2 / M期百分比减少。 72h后,治疗组出现凋亡峰,高剂量组凋亡率为30.94±1.74%; 48h后,治疗组中的ROS随高剂量组增加77.7±4.5%; Δψm从上面的高剂量组减少77.8±1.9%,可以看出,芦笋皂苷对Hepg2细胞具有相对强烈的抑制作用,并且所涉及的机制必须符合其在增加细胞内RO的生产中的作用,其中导致线粒体膜电位的降低,从而引发诱导HepG2细胞凋亡的凋亡机制。

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