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静磁场通过调节活性氧行为远程增强阿霉素的效率。

The Static Magnetic Field Remotely Boosts the Efficiency of Doxorubicin through Modulating ROS Behaviors.

机构信息

Department of Biophysics, Faculty of Biological Sciences, Tarbiat Modares University (TMU), Tehran, Iran.

Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University (TMU), Tehran, Iran.

出版信息

Sci Rep. 2018 Jan 17;8(1):990. doi: 10.1038/s41598-018-19247-8.

Abstract

Exposure to magnetic field (MF) can affect cellular metabolism remotely. Cardio-toxic effects of Doxorubicin (DOXO) have limited clinical uses at high dose. MF due to its effect on reactive oxygen species (ROS) lifetime, may provide a suitable choice to boost the efficacy of this drug at low dose. Here, we investigated the potential effects of homogenous static magnetic field (SMF) on DOXO-induced toxicity and proliferation rate of cancer cells. The results indicated that SMF similar to DOXO decreased the cell viability as well as the proliferation rate of MCF-7 and HFF cells. Moreover, combination of 10 mT SMF and 0.1 µM DOXO decreased the viability and proliferation rate of cancer and normal cells in a synergetic manner. In spite of high a GSH level in cancer cell, SMF boosts the generation and lifetime of ROS at low dose of DOXO, and overcame to GSH mediated drug resistance. The results also confirmed that SMF exposure decreased 50% iron content of cells, which is attributed to iron homeostasis. In conclusion, these findings suggest that SMF can decrease required dose of chemotherapy drugs such as DOXO and thereby decrease their side effect.

摘要

磁场(MF)暴露可以远程影响细胞代谢。阿霉素(DOXO)的心脏毒性作用在高剂量下的临床应用有限。MF 由于其对活性氧(ROS)寿命的影响,可能是在低剂量下提高这种药物疗效的合适选择。在这里,我们研究了均匀静磁场(SMF)对 DOXO 诱导的癌细胞毒性和增殖率的潜在影响。结果表明,SMF 与 DOXO 相似,降低了 MCF-7 和 HFF 细胞的活力和增殖率。此外,10 mT SMF 和 0.1 µM DOXO 的组合以协同方式降低了癌细胞和正常细胞的活力和增殖率。尽管癌细胞中的 GSH 水平较高,但 SMF 在低剂量 DOXO 下会促进 ROS 的产生和寿命,并克服 GSH 介导的耐药性。结果还证实,SMF 暴露会降低细胞中 50%的铁含量,这归因于铁的动态平衡。总之,这些发现表明,SMF 可以降低化疗药物(如 DOXO)的所需剂量,从而降低其副作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd61/5772617/865ed2c80d8e/41598_2018_19247_Fig1_HTML.jpg

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