考虑到蓝光光生物调节 (PBM) 在各种癌症模型中的已知有效性，研究蓝光光生物调节 (PBM) 在 OS 细胞中诱导铁死亡（一种新型的受调节细胞死亡形式）的潜力。在这项研究中，我们将人类 OS 细胞系 HOS 和 MG63 暴露在不同辐照度下的不同波长（420、460 和 480 nm）的蓝光下，并检查细胞反应，例如活力、细胞凋亡、活性氧 (ROS) 水平）和线粒体膜电位（MMP）。采用转录组测序来揭示蓝光诱导效应的分子机制，并通过定量实时 PCR (qRT-PCR) 进行验证。我们的研究结果揭示了细胞活力的波长和时间依赖性下降，并伴随着细胞凋亡和氧化应激的增加。转录组分析确定了与铁死亡、氧化应激和铁代谢相关的基因的差异表达，并通过 qRT-PCR 进一步验证。这些结果表明铁死亡是蓝光诱导 OS 细胞死亡的一个重要机制，可能是由 ROS 生成和铁稳态破坏介导的。此外，在蓝光照射诱导的 MG63 细胞中观察到不完全的应激反应。因此，蓝光 PBM 有望成为 OS 临床研究中的一种治疗方法。然而，对其潜在机制的进一步探索仍然势在必行。版权所有 © 2024。由 Elsevier B.V. 出版。

To investigate the potential of blue light photobiomodulation (PBM) in inducing ferroptosis, a novel form of regulated cell death, in OS cells, considering its known effectiveness in various cancer models. In this investigation, we exposed human OS cell lines, HOS and MG63, to different wavelengths (420, 460 and 480 nm) of blue light at varying irradiances, and examined cellular responses such as viability, apoptosis, levels of reactive oxygen species (ROS), and mitochondrial membrane potential (MMP). Transcriptome sequencing was employed to unravel the molecular mechanisms underlying blue light-induced effects, with validation via quantitative real-time PCR (qRT-PCR). Our findings revealed a wavelength- and time-dependent decrease in cell viability, accompanied by increased apoptosis and oxidative stress. Transcriptomic analysis identified differential expression of genes associated with ferroptosis, oxidative stress, and iron metabolism, further validated by qRT-PCR. These results implicated ferroptosis as a significant mechanism in the blue light-induced death of OS cells, potentially mediated by ROS generation and disruption of iron homeostasis. Also, An incomplete stress response was observed in MG63 cells induced by blue light exposure. Hence, blue light PBM holds promise as a therapeutic approach in OS clinical investigations; however, additional exploration of its underlying mechanisms remains imperative.Copyright © 2024. Published by Elsevier B.V.