Bartos Adam, Grondin Yohann, Bortoni Magda E, Ghelfi Elisa, Sepulveda Rosalinda, Carroll James, Rogers Rick A
Harvard University - Harvard T.H. Chan School of Public Health, Molecular and Integrative Physiological Sciences - Department of Environmental Health, Building 1, 665 Huntington Ave, Boston, MA, 02115, USA.
THOR Photomedicine Ltd, Chesham, HP5 1LF, United Kingdom.
J Biophotonics. 2016 Dec;9(11-12):1125-1135. doi: 10.1002/jbio.201500209. Epub 2016 Jan 21.
Hearing loss is a serious occupational health problem worldwide. Noise, aminoglycoside antibiotics and chemotherapeutic drugs induce hearing loss through changes in metabolic functions resulting in sensory cell death in the cochlea. Metabolic sequelae from noise exposure increase production of nitric oxide (NO) and Reactive Oxygen Species (ROS) contributing to higher levels of oxidative stress beyond the physiologic threshold levels of intracellular repair. Photobiomodulation (PBM) therapy is a light treatment involving endogenous chromophores commonly used to reduce inflammation and promote tissue repair. Near infrared light (NIR) from Light Emitting Diodes (LED) at 810 nm wavelength were used as a biochemical modulator of cytokine response in cultured HEI-OC1 auditory cells placed under oxidative stress. Results reported here show that NIR PBM at 810 nm, 30 mW/cm , 100 seconds, 1.0 J, 3 J/cm altered mitochondrial metabolism and oxidative stress response for up to 24 hours post treatment. We report a decrease of inflammatory cytokines and stress levels resulting from NIR applied to HEI-OC1 auditory cells before treatment with gentamicin or lipopolysaccharide. These results show that cells pretreated with NIR exhibit reduction of proinflammatory markers that correlate with inhibition of mitochondrial superoxide, ROS and NO in response to continuous oxidative stress challenges. Non-invasive biomolecular down regulation of proinflammatory intracellular metabolic pathways and suppression of oxidative stress via NIR may have the potential to develop novel therapeutic approaches to address noise exposure and ototoxic compounds associated with hearing loss.
听力损失是全球范围内一个严重的职业健康问题。噪声、氨基糖苷类抗生素和化疗药物通过代谢功能的改变导致耳蜗感觉细胞死亡，从而引发听力损失。噪声暴露引起的代谢后遗症会增加一氧化氮（NO）和活性氧（ROS）的产生，导致氧化应激水平升高，超过细胞内修复的生理阈值水平。光生物调节（PBM）疗法是一种利用内源性发色团的光疗方法，常用于减轻炎症和促进组织修复。波长为810 nm的发光二极管（LED）发出的近红外光（NIR）被用作置于氧化应激下的培养HEI-OC1听觉细胞中细胞因子反应的生化调节剂。此处报告的结果表明，810 nm、30 mW/cm²、100秒、1.0 J、3 J/cm²的近红外光生物调节在处理后长达24小时内改变了线粒体代谢和氧化应激反应。我们报告，在用庆大霉素或脂多糖处理之前，将近红外光应用于HEI-OC1听觉细胞会导致炎症细胞因子和应激水平降低。这些结果表明，用近红外光预处理的细胞表现出促炎标志物减少，这与在持续氧化应激挑战下线粒体超氧化物、活性氧和一氧化氮的抑制相关。通过近红外光对促炎细胞内代谢途径进行非侵入性生物分子下调以及抑制氧化应激，可能有潜力开发新的治疗方法来应对与听力损失相关的噪声暴露和耳毒性化合物。
