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Pentoxifylline induces apoptosis of HepG2 cells by reducing reactive oxygen species production and activating the MAPK signaling

机译：Pentoxifylline通过减少反应性氧物种生产并激活MAPK信号传导来诱导HepG2细胞的凋亡

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摘要

Abstract Aims Pentoxifylline (PTX) is a methylxanthine derivative and has potent anti-tumor activity. This study aimed at investigating the anti-HCC effects of PTX and associated molecular mechanisms. Main methods The effects of varying doses of PTX on viability, cell cycle and apoptosis of HepG2 cells were determined by MTT and flow cytometry, respectively. The effects of PTX on the production of reactive oxygen species (ROS), expression of pro- and anti-apoptotic regulators and activation of the MAPK signaling in HepG2 cells were analyzed by flow cytometry and Western blot assays. The effects of PTX on the growth of implanted HepG2 cells and their apoptosis in mice were examined. Key findings Our results indicated that PTX inhibited proliferation of HepG2 cells and induced HepG2 cell cycle arrest at G0/G1 phase and apoptosis in a dose- and time-dependent manner. Treatment with PTX reduced levels of ROS and Bcl-X L expression, but increased caspase 3 and caspase 9 expression and JNK and ERK1/2 phosphorylation in HepG2 cells. Pre-treatment with n -acetyl- l -cysteine (NAC), a ROS scavenger, enhanced PTX-mediated cell cycle arrest, apoptosis and the JNK and ERK MAPK activation, while pre-treatment with SP600125 or PD98509 attenuated PTX-mediated effects in HepG2 cells. Treatment with PTX inhibited the growth of implanted HCC and promoted HCC apoptosis in mice. Significance Our data demonstrate that PTX inhibits proliferation of HepG2 cells and induces HepG2 cell apoptosis by attenuating ROS production and enhancing the MAPK activation in HepG2 cells. ]]>
机译：摘要目的偏毒素碱（PTX）是甲基黄嘌呤衍生物并具有有效的抗肿瘤活性。本研究旨在研究PTX和相关分子机制的抗HCC效应。主要方法分别通过MTT和流式细胞术测定不同剂量的PTX对活力，细胞周期和凋亡的影响。通过流式细胞术和蛋白质印迹测定分析PTX对反应性氧物质（ROS）的产生，抗凋亡调节剂的表达和MAPK信号传导的影响的影响。研究了PTX对植入HepG2细胞生长及其小鼠细胞凋亡的影响。主要发现我们的结果表明，PTX抑制了HepG2细胞的增殖，并以剂量​​和时间依赖的方式诱导G0 / G1相的HepG2细胞周期停滞。用PTX治疗降低ROS和BCL-X L表达水平，但在HepG2细胞中增加了Caspase 3和Caspase 9表达和JNK和ERK1 / 2磷酸化。用N-乙酰基-1-胞嘧啶（NAC），ROS清除剂，增强的PTX介导的细胞周期停滞，细胞凋亡和JNK和ERK MAPK活化，同时用SP600125或PD98509进行预处理，抑制PTX介导的效果hepg2细胞。用PTX治疗抑制植入的HCC的生长并促进小鼠中的HCC凋亡。重要性我们的数据表明，PTX通过衰减ROS产生并增强HepG2细胞中的MAPK激活来抑制HepG2细胞的增殖并诱导HepG2细胞凋亡。 ]]>

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  • 来源
    《Life sciences》 |2017年第2017期|共9页
  • 作者

    Yan Wang; Lei Dong; Jing Li; Miaosha Luo; Boxin Shang;

  • 作者单位

    Department of Gastroenterology The Second Affiliated Hospital of Xi'an Jiaotong University;

    Department of Gastroenterology The Second Affiliated Hospital of Xi'an Jiaotong University;

    Department of Gastroenterology The Second Affiliated Hospital of Xi'an Jiaotong University;

    Department of Gastroenterology The Second Affiliated Hospital of Xi'an Jiaotong University;

    Department of Gastroenterology The Second Affiliated Hospital of Xi'an Jiaotong University;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 医药、卫生;
  • 关键词

    Pentoxifylline; Liver cancer; MAPK pathway; ROS; Caspase 3; Caspase 9; BcL-XL;

    机译：pentoxifylline;肝癌;Mapk途径;ROS;Caspase 3;Caspase 9;Bcl-XL;

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