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9 March 2012 Low level laser therapy reduces oxidative stress in cortical neurons in vitro
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Proceedings Volume 8211, Mechanisms for Low-Light Therapy VII; 821103 (2012) https://doi.org/10.1117/12.912948
Event: SPIE BiOS, 2012, San Francisco, California, United States
Abstract
It is accepted that the mechanisms of low level laser therapy (LLLT) involves photons that are absorbed in the mitochondria of cells and lead to increase of mitochondrial metabolism resulting in more electron transport, increase of mitochondrial membrane potential, and more ATP production. Intracellular calcium changes are seen that correlate with mitochondrial stimulation. The situation with two other intermediates is more complex however: reactive oxygen species (ROS) and nitric oxide (NO). Evidence exists that low levels of ROS are produced by LLLT in normal cells that can be beneficial by (for instance) activating NF-kB. However high fluences of light can produce large amounts of ROS that can damage the cells. In oxidatively stressed cells the situation may be different. We exposed primary cultured cortical neurons to hydrogen peroxide (H2O2) or cobalt chloride (CoCl2) oxidative insults in the presence or absence of LLLT (810-nm laser at 0.3 or 3 J/cm2). Cell viability of cortical neurons was determined by lactate dehydrogenase assay. ROS in neurons was detected using an ROS probe, MitoRox with confocal microscopy. Results showed that LLLT dose-dependently reversed ROS production and protected cortical neurons against H2O2 or CoCl2 induced oxidative injury in cultured cortical neurons. Conclusion: LLLT can protect cortical neurons against oxidative stress by reversing the levels of ROS.
© (2012) COPYRIGHT Society of Photo-Optical Instrumentation Engineers (SPIE). Downloading of the abstract is permitted for personal use only.
Ying-Ying Huang, Clark E. Tedford, Thomas McCarthy, and Michael R. Hamblin "Low level laser therapy reduces oxidative stress in cortical neurons in vitro", Proc. SPIE 8211, Mechanisms for Low-Light Therapy VII, 821103 (9 March 2012); https://doi.org/10.1117/12.912948
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