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投稿时间：2018-07-03
投稿时间：2018-07-03
中文摘要: 探讨马齿苋多糖（polysaccharide of Portulaca oleracea L.，POP-A）对HepG2细胞的抑制作用及作用机制。体外培养HepG2细胞，分别用不同浓度的POP-A处理细胞，采用四甲基偶氮唑盐 [3-（4，5-dimethyl-2-thiazolyl）-2，5-diphenyl-2-H-tetrazolium bromide，MTT]法、荧光定性定量法、免疫印迹法以及反转录聚合酶链式反应（reverse transcription-PCR，RT-PCR）法等检测POP-A对HepG2细胞存活率、线粒体膜电位、细胞内钙离子以及相关凋亡蛋白与基因表达的影响。结果表明：当POP-A浓度为1.25、2.5、5 mg/mL时，POP-A能够显著抑制HepG2肝癌细胞、降低线粒体膜电位、增加细胞内的钙离子浓度、提高p53和Bax的基因及蛋白表达。说明POP-A有抑制HepG2肝癌细胞的作用，其作用机制与促进HepG2细胞凋亡有关。
Abstract:To explore the inhibitory effect and primary mechanism of polysaccharide from Portulaca oleracea L.（POP-A）on growth of HepG2 cells.HepG2 cells were cultured in vitro.The effect of POP-A on cells viability，mitochondrial membrane potential，intracellular Ca2+levels and the expression levels of related apoptotic proteins and gene of HepG2 cells were studied by 3-（4，5-dimethyl-2-thiazolyl）-2，5-diphenyl-2-H-tetrazolium bromide （MTT）assay，fluorescence quantitative analysis，Western blotting and reverse transcription-PCR（RT-PCR）.Results showed that 1.25，2.5，5 mg/mL POP-A significantly inhibited the cell viability of HepG2 cells，decreased mitochondrial membrane potential，increased intracellular Ca2+levels and increased the gene and protein expression levels of p53 and Bax.These results suggested that POP-A could inhibit the apoptosis of HepG2 cells，and its mechanism was related to the promotion of apoptosis of HepG2 cells.
文章编号：201903007 中图分类号： 文献标志码：
基金项目:国家自然科学基金项目（31360376）；江西省自然科学基金项目（20132BAB205091）；本科生科研基金项目（201711318017）
| Author Name | Affiliation |
| HU Qing-juan，NIU Qing-chuan，SONG Hao，BAI Shu-yu，HE Wen-jie，LI Yu-ping | School of Life Science，Jiangxi Science＆Technology Normal University，Nanchang 330013，Jiangxi，China |
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