Position: Home > Articles > Apoptosis Mechanism of SMMC-7721 Cells Induced by Polysaccharides from the Liquid Submerged Fermentation of Hericium caput-medusae
Journal of Jilin Agricultural University
2013,35
(5)
30-34
小刺猴头液体深层发酵浸膏多糖诱导SMMC-7721细胞凋亡的机制
作 者：
高梓越;刘小腊;李沐;余涛
单 位：
吉林农业大学生命科学学院
关键词：
HFP;细胞凋亡;线粒体膜电位;Caspase-9;Caspase-3
摘 要：
用荧光染色观察小刺猴头菌液体深层发酵浸膏多糖(HFP)对SMMC-7721细胞核形变化的影响;用流式细胞仪研究HFP对SMMC-7721细胞的诱导凋亡作用和细胞周期的影响,并通过JC-1荧光染色法观察线粒体膜电位变化和ELISA法检测Caspase-9和Caspase-3活性来探讨HFP诱导人肝癌细胞SMMC-7721凋亡作用的机制。结果表明:不同浓度的HFP作用24 h后,SMMC-7721细胞呈现典型细胞凋亡特征,细胞周期阻滞于G2/M期,同时引起线粒体膜电位降低,而Caspase-9和Caspase-3活性增高。说明HFP具有明显的诱导SMMC-7721细胞凋亡作用,其机制与引起细胞周期阻滞有关,而且线粒体途径也是其诱导肿瘤细胞凋亡的机制之一。
译 名：
Apoptosis Mechanism of SMMC-7721 Cells Induced by Polysaccharides from the Liquid Submerged Fermentation of Hericium caput-medusae
作 者：
GAO Zi-yue;LIU Xiao-la;LI Mu;YU Tao;School of Life Sciences,Jilin Agricultural University;
关键词：
HFP;;apoptosis;;mitochondrial membrane potential;;Caspase-3;;Caspase-9
摘 要：
To explore the apoptosis mechanism of SMMC-7721 cell induced by polysaccharides from the liquid submerged fermentation extract of Hericium caput-medusae, the fluorescent microscope was utilized to observe the morphological changes of apoptosis. The effects of induced apoptosis and cell cycle were studied with flow cytometry. The method of JC-1 fluorescent staining was utilized to observe the changes of mitochondrial membrane potential and the activity of Caspase-9 and Caspase-3 was determined by ELISA assay. The results showed that typical morphological changes of apoptosis in SMMC-7721 cancer cells treated with HFP after 24 h could be observed with the fluorescent microscope. By flow cytometry analysis,cells were blocked in G2/M phase and mitochondrial membrane potential was declined,but the activity of Caspase-9 and Caspase-3 increased. HFP could markedly induce apoptosis in SMMC-7721 hepatocellular cancer cells. The mechanism might be not only related to cell cycle arrest but also related to mitoc-hondrial pathway.
导出引用
计量
文章访问数: 7
HTML全文浏览量: 0
PDF下载量: 0
所属期刊
