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Antitumor activity of a sulfated polysaccharide from Enteromorpha intestinalis targeted against hepatoma through mitochondrial pathway.

机译:小肠肠Enter中硫酸化多糖通过线粒体途径靶向肝癌的抗肿瘤活性。

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摘要

A sulfated polysaccharide (EI-SP), extracted from Enteromorpha intestinalis that is a kind of algae, is found to have anticancer activity. This study was designed to investigate the anti-tumor effect of EI-SP on human hepatoma HepG2 cell line and its possible mechanisms. An MTT assay showed that EI-SP could specifically inhibit the growth of human hepatoma HepG2 cells in a dose-dependent manner. Analysis by flow cytometry indicated that the apoptosis of tumor cells increased after treatment with EI-SP in range of 100-400 μg/ml. Furthermore, Western blot analysis showed that EI-SP treatment led to decreased protein expression of Bcl-2 and an increase in Bax, cleaved caspase-3, cleaved caspase-9 and cleaved poly(ADP-ribose) polymerase (PARP). Moreover, it was found that EI-SP caused a loss of mitochondrial membrane potential (Δψ m) and the release of cytochrome c to the cytosol. Collectively, our results showed that the EI-SP induces apoptosis in HepG2 cells involving a caspases-mediated mitochondrial signalling pathway.
机译:从一种肠藻肠小肠虫中提取的硫酸多糖(EI-SP)具有抗癌活性。本研究旨在探讨EI-SP对人肝癌HepG2细胞株的抗肿瘤作用及其可能的机制。 MTT分析表明,EI-SP可以剂量依赖性方式特异性抑制人肝癌HepG2细胞的生长。流式细胞仪分析表明,用EI-SP处理后,在100-400μg/ ml范围内,肿瘤细胞的凋亡增加。此外,蛋白质印迹分析表明,EI-SP处理导致Bcl-2的蛋白表达降低,并且Bax,裂解的caspase-3,裂解的caspase-9和裂解的聚(ADP-核糖)聚合酶(PARP)升高。此外,发现EI-SP引起线粒体膜电位(Δψm)的损失以及细胞色素c向细胞质的释放。总体而言,我们的结果表明,EI-SP诱导了涉及半胱氨酸蛋白酶介导的线粒体信号传导途径的HepG2细胞凋亡。

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