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首页> 外文期刊>Oncology reports >Polysaccharide sulphated derivative from Aconitum coreanum induces cell apoptosis in the human brain glioblastoma U87MG cell line via the NF-kappa B/Bcl-2 cell apoptotic signaling pathway
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Polysaccharide sulphated derivative from Aconitum coreanum induces cell apoptosis in the human brain glioblastoma U87MG cell line via the NF-kappa B/Bcl-2 cell apoptotic signaling pathway

机译:来自Aconitum Coreanum的多糖硫酸化衍生物通过NF-Kappa B / Bcl-2细胞凋亡信号通路诱导人脑胶质细胞瘤U87mg细胞系中的细胞凋亡

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摘要

In a previous study, our team preliminarily investigated the bioefficacy of an extracted polysaccharide from the medicinal plant Aconitum coreanum (ACP1). In the present study, we further evaluated the antitumor efficacy of an ACP1 sulphated derivative (ACP1-s) in the human brain glioblastoma U87MG cell line. Cell viability assay and flow cytometry results demonstrated that 400, 800 and 1,600 mu g/ml ACP1-s induced cell growth inhibition and cell apoptosis. We then investigated the underlying molecular mechanism of the ACP1-s induced cell apoptosis and found that the NF-kappa B/Bcl-2 cell apoptotic signaling pathway was involved. Following treatment with ACP1-s, the expression of IB in U87MG cells was significantly upregulated, whereas the level of NF-kappa B and the ratio of Bcl-2/Bax was significantly decreased. The level of cleaved caspase-3 was increased accordingly. When we introduced exogenous p65 protein into the U87MG cells, the ACP1-s-induced cell growth inhibition and cell apoptosis were partially neutralized, and the expression of the anti-apoptotic gene Bcl-2 was recovered accordingly. These findings suggest the potential value of ACP1-s as a novel therapeutic agent for the treatment of glioblastoma.
机译:在以前的一项研究中,我们的团队初步研究了来自药用植物Aconitum Coreanum(ACP1)的提取的多糖的生物效率。在本研究中,我们进一步评估了在人脑胶质母细胞瘤U87mg细胞系中ACP1硫酸化衍生物(ACP1-S)的抗肿瘤功效。细胞活力测定和流式细胞术的结果表明,400,800和1,600μg/ ml ACP1-S诱导的细胞生长抑制和细胞凋亡。然后,我们研究了ACP1-S诱导细胞凋亡的潜在分子机制,发现涉及NF-Kappa B / Bcl-2细胞凋亡信号通路。用ACP1-S处理后,显着上调U87MG细胞中的IB的表达,而NF-Kappa B的水平和Bcl-2 / Bax的比例显着降低。相应地增加了切割的Caspase-3水平。当我们将外源p65蛋白引入U87mg细胞时,部分中和ACP1-S诱导的细胞生长抑制和细胞凋亡,相应地回收抗凋亡基因Bcl-2的表达。这些发现表明ACP1-S作为治疗胶质母细胞瘤的新型治疗剂的潜在价值。

著录项

  • 来源
    《Oncology reports》 |2018年第3期|共6页
  • 作者单位

    Jilin Univ China Japan Union Hosp Dept Neurosurg 126 XianTai St Changchun 130033 Jilin;

    Jilin Univ Dept Pediat Surg Hosp 1 Changchun 130021 Jilin Peoples R China;

    Changchun Univ Chinese Med Dept Dermatol Affiliated Hosp Changchun 130021 Jilin Peoples R China;

    Jilin Univ China Japan Union Hosp Dept Gastrointestinal Colorectal Surg Changchun 130033 Jilin;

    Jilin Univ China Japan Union Hosp Dept Neurosurg 126 XianTai St Changchun 130033 Jilin;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 肿瘤学;
  • 关键词

    glioblastoma; polysaccharide; cell apoptosis;

    机译:胶质母细胞;多糖;细胞凋亡;

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