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静磁场降低细胞内 ROS 水平并保护细胞免受过氧化物诱导的损伤:过氧化氢酶的建议作用。

Static Magnetic Field Reduces Intracellular ROS Levels and Protects Cells Against Peroxide-Induced Damage: Suggested Roles for Catalase.

机构信息

Department of Fundamental Chemistry, Institute of Chemistry, University of São Paulo, Av. Prof. Lineu Prestes 748, São Paulo, 05508-000, Brazil.

Department of Biochemistry, Institute of Chemistry, University of São Paulo, Av. Prof. Lineu Prestes 748, São Paulo, 05508-000, Brazil.

出版信息

Neurotox Res. 2023 Dec 14;42(1):2. doi: 10.1007/s12640-023-00679-8.

Abstract

A feature in neurodegenerative disorders is the loss of neurons, caused by several factors including oxidative stress induced by reactive oxygen species (ROS). In this work, static magnetic field (SMF) was applied in vitro to evaluate its effect on the viability, proliferation, and migration of human neuroblastoma SH-SY5Y cells, and on the toxicity induced by hydrogen peroxide (HO), tert-butyl hydroperoxide (tBHP), HO/sodium azide (NaN) and photosensitized oxidations by photodynamic therapy (PDT) photosensitizers. The SMF increased almost twofold the cell expression of the proliferation biomarker Ki-67 compared to control cells after 7 days of exposure. Exposure to SMF accelerated the wound healing of scratched cell monolayers and significantly reduced the HO-induced and the tBHP-induced cell deaths. Interestingly, SMF was able to revert the effects of NaN (a catalase inhibitor), suggesting an increased activity of catalase under the influence of the magnetic field. In agreement with this hypothesis, SMF significantly reduced the oxidation of DCF-H2, indicating a lower level of intracellular ROS. When the redox imbalance was triggered through photosensitized oxidation, no protection was observed. This observation aligns with the proposed role of catalase in cellular proctetion under SMF.  Exposition to SMF should be further validated in vitro and in vivo as a potential therapeutic approach for neurodegenerative disorders.

摘要

神经退行性疾病的一个特征是神经元的丧失,这是由多种因素引起的,包括活性氧(ROS)诱导的氧化应激。在这项工作中,体外应用静磁场(SMF)来评估其对人神经母细胞瘤 SH-SY5Y 细胞活力、增殖和迁移的影响,以及对过氧化氢(HO)、叔丁基过氧化物(tBHP)、HO/叠氮化钠(NaN)诱导的毒性和光动力疗法(PDT)光敏剂的光氧化的影响。与对照细胞相比,暴露于 SMF 7 天后,细胞增殖生物标志物 Ki-67 的表达几乎增加了两倍。暴露于 SMF 加速了划痕细胞单层的愈合,并且显著降低了 HO 诱导和 tBHP 诱导的细胞死亡。有趣的是,SMF 能够逆转 NaN(过氧化氢酶抑制剂)的作用,这表明在磁场的影响下过氧化氢酶的活性增加。与这一假设一致,SMF 显著降低了 DCF-H2 的氧化,表明细胞内 ROS 的水平较低。当通过光氧化引发氧化还原失衡时,没有观察到保护作用。这一观察结果与过氧化氢酶在 SMF 下对细胞保护的作用相一致。SMF 的体外和体内进一步验证应作为神经退行性疾病的潜在治疗方法。

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