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首页> 外文期刊>Photodiagnosis and Photodynamic Therapy >Possible mechanism of heme oxygenase-1 expression in rat malignant meningioma KMY-J cells subjected to talaporfin sodium-mediated photodynamic therapy
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Possible mechanism of heme oxygenase-1 expression in rat malignant meningioma KMY-J cells subjected to talaporfin sodium-mediated photodynamic therapy

机译：大鼠恶性脑膜瘤KMY-J细胞的血红素氧合酶-1表达的可能机制对术治疗钠钠介导的光动力治疗

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摘要

Background: We previously demonstrated that heme oxygenase-1 (HO-1) induction may contribute to a protective response against photodynamic therapy (PDT) using talaporfin sodium (TS) in rat malignant meningioma KMY-J cells. In the present study, we examined the mechanism of HO-1 induction by PDT with TS (TS-PDT) in KMY-J cells.Methods: KMY-J cells were incubated with 25 mu M TS for 2 h and then exposed to 664 nm diode laser irradiation at 1 J/cm(2). The gene and protein expression levels of HO-1 and hypoxia-inducible factor-1 alpha (HIF-1 alpha) were determined by real-time RT-PCR and western blot analysis, respectively. Cell viability was measured using the cell counting kit-8 assay.Results: mRNA and protein levels of HO-1 in KMY-J cells were increased significantly at 3, 6, and 9 h after laser irradiation and the increased mRNA level of HO-1 was decreased by antioxidant N-acetyl cysteine treatment. The protein level of HIF-la, which mediates transcriptional activation of the HO-1 gene, was increased significantly at 1 h after laser irradiation. Additionally, induction of mRNA expression of HO-1 by TS-PDT was diminished by HIF-1 a inhibitor echinomycin. We also demonstrated that echinomycin significantly augmented the cytotoxic effect of TS-PDT.Conclusions: Our findings indicate that TS-PDT may induce HO-1 expression via reactive oxygen species production and then HIF-1 pathway activation in KMY-J cells, and the HO-1 induction may cause attenuation of the therapeutic effect of TS-PDT.
机译：背景：我们之前证明血红素氧酶-1（HO-1）诱导可能有助于使用大鼠恶性脑膜瘤KMY-J细胞中的Talaporfin钠（TS）对光动力治疗（PDT）的保护响应。在本研究中，我们在Kmy-J细胞中检查了PDT的HO-1诱导的机制。方法：KMY-J细胞与25μmTS孵育2小时，然后暴露于664 NM二极管激光照射为1J / cm（2）。通过实时RT-PCR和Western印迹分析测定HO-1和缺氧诱导因子-1α（HIF-1α）的基因和蛋白表达水平。使用细胞计数试剂盒-8 assay测量细胞活力。结果：激光照射后3,6和9小时，KMY-J细胞的HO-1的mRNA和蛋白质水平显着增加，并且HO-增加的mRNA水平通过抗氧化剂N-乙酰半胱氨酸处理减少1。在激光照射后1小时，介导HO-1基因转录激活的HIF-LA的蛋白质水平在1小时内显着增加。另外，通过HIF-1抑制剂海螺瘤素减少了TS-PDT的HO-1 mRNA表达的诱导。我们还证明了echinomycin显着增强了TS-PDT的细胞毒性作用：结论：我们的发现表明，TS-PDT可以通过反应性氧物种生产诱导HO-1表达，然后在KMY-J细胞中诱导HIF-1途径激活。 HO-1诱导可能导致TS-PDT治疗效果的衰减。

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  • 来源
    《Photodiagnosis and Photodynamic Therapy》 |2020年第12期|102009.1-102009.6|共6页
  • 作者

    Takahashi Tsutomu; Misawa Suzuka; Suzuki Saki; Saeki Nanako; Shinoda Yo; Tsuneoka Yayoi; Akimoto Jiro; Fujiwara Yasuyuki;

  • 作者单位

    Tokyo Univ Pharm & Life Sci Sch Pharm Dept Environm Hlth 1432-1 Horinouchi Hachioji Tokyo 1920392 Japan;

    Tokyo Univ Pharm & Life Sci Sch Pharm Dept Environm Hlth 1432-1 Horinouchi Hachioji Tokyo 1920392 Japan;

    Tokyo Univ Pharm & Life Sci Sch Pharm Dept Environm Hlth 1432-1 Horinouchi Hachioji Tokyo 1920392 Japan;

    Tokyo Univ Pharm & Life Sci Sch Pharm Dept Environm Hlth 1432-1 Horinouchi Hachioji Tokyo 1920392 Japan;

    Tokyo Univ Pharm & Life Sci Sch Pharm Dept Environm Hlth 1432-1 Horinouchi Hachioji Tokyo 1920392 Japan;

    Tokyo Univ Pharm & Life Sci Sch Pharm Dept Environm Hlth 1432-1 Horinouchi Hachioji Tokyo 1920392 Japan;

    Tokyo Med Univ Dept Neurosurg Shinjuku Ku 6-7-1 Nishi Shinjuku Tokyo 1600023 Japan;

    Tokyo Univ Pharm & Life Sci Sch Pharm Dept Environm Hlth 1432-1 Horinouchi Hachioji Tokyo 1920392 Japan;

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  • 正文语种 eng
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  • 关键词

    Photodynamic therapy; Talaporfin sodium; Hypoxia-inducible factor-1; Heme oxygenase-1; Malignant meningioma KMY-J cell;

    机译：光动力疗法;Talaporfin钠;缺氧诱导因子-1;血红素氧合酶-1;恶性脑膜瘤KMY-J细胞;

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