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文冠果种仁总皂苷诱导肝癌HepG2细胞凋亡的实验研究 被引量:5

Research of hepatocellular carcinoma HepG2 cell apoptosis induced by total saponins of Xanthoceras sorbifolia bunge kernel
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摘要 用文冠果种仁总皂苷(the total saponins from Xanthoceras sorbifolia bunge kernel,XSTS)处理人肝癌HepG2细胞,探讨其诱导HepG2细胞凋亡的分子机制。利用JC-1荧光探针检测HepG2细胞线粒体膜电势的变化,运用流式细胞仪和比色法检测细胞内活性氧和一氧化氮水平,用Western blot法检测XSTS对细胞凋亡特征蛋白的影响。结果发现:质量浓度为8~12 mg/L的XSTS可诱导HepG2细胞发生线粒体介导的内源性凋亡,该途径受到PI3K/Akt通路调控;且XSTS可通过激发氧化应激而非硝化应激来诱导细胞凋亡。 The molecular mechanism of HepG2 cell apoptosis induced by the total saponins from Xanthoceras sorbifolia bunge kernel(XSTS)was explored through XSTS treatment on the human hepatocellular carcinoma HepG2 cells.Firstly,the changes of mitochondrial membrane potential in HepG2 cells were measured by the fluorescence probe of JC-I.Then,the levels of reactive oxygen species and NO content in the HepG2 cells were detected using flow cytometry and colorimetric methods.Finally,the Western blot method was used to detect the effect of XSTS on the apoptosis-related proteins in HepG2 cells.Results showed that the apoptosis of cells was achieved by mitochondrial-mediated endogenous apoptotic pathway after XSTS treatment(concentration of 8~12 mg/L)on HepG2 cells,and this pathway was mediated by PI3K/Akt approach.At the same time,the XSTS can stimulate cells to produced oxidative stress rather than nitrification stress and induce the apoptosis of HepG2 cells.The experimental result provides a theoretical basis for exploring the anticancer activity of Xanthoceras sorbifolia bunge kernel saponins.
作者 雷佳蕾 张志宇 杨天歌 邓红 马婧 孟永宏 LEI Jialei;ZHANG Zhiyu;YANG Tiange;DENG Hong;MA Jing;MENG Yonghong(School of Food Engineering and Nutritional Science,Shaanxi Normal University,Xi′an 710119,Shaanxi,China)
出处 《陕西师范大学学报(自然科学版)》 CAS CSCD 北大核心 2020年第1期80-86,共7页 Journal of Shaanxi Normal University:Natural Science Edition
基金 陕西省自然科学基金(2013JM4036) 农业部产业体系项目(CARS-28)
关键词 文冠果种仁总皂苷 HEPG2细胞 细胞凋亡 线粒体途径 PI3K/AKT通路 total saponins of Xanthoceras sorbifolia bunge kernel HepG2 cells cell apoptosis mitochondrial pathway PI3K/Akt pathway
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