Photobiomodulation preconditioning prevents cognitive impairment in a neonatal rat model of hypoxia‐ischemia |
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| Authors: | Luodan Yang Yan Dong Chongyun Wu Yong Li Yichen Guo Baocheng Yang Xuemei Zong Michael R Hamblin Timon C‐Y Liu Quanguang Zhang |
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| Institution: | 1. Laboratory of Laser Sports Medicine, College of Physical Education and Sports Science, South China Normal University, Guangzhou, China;2. Department of Neuroscience & Regenerative Medicine, Medical College of Georgia, Augusta University, Augusta, Georgia;3. Wellman Center for Photomedicine, Massachusetts General Hospital, Boston, Massachusetts;4. Department of Dermatology, Harvard Medical School, Boston, Massachusetts;5. Harvard‐MIT Division of Health Sciences and Technology, Cambridge, Massachusetts;6. Quanguang Zhang, Laboratory of Laser Sports Medicine, College of Physical Education and Sports Science, South China Normal University, University Town, Guangzhou GD 510006, China.;7. Timon C.‐Y. Liu, Laboratory of Laser Sports Medicine, College of Physical Education and Sports Science, South China Normal University, University Town, Guangzhou GD 510006, China.;8. Michael R. Hamblin, Wellman Center for Photomedicine, Massachusetts General Hospital, Boston, MA 02114.;9. https://orcid.org/0000-0001-6499-7952 |
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| Abstract: | Neonatal hypoxia‐ischemia (HI) injury caused by oxygen deprivation is the most common cause of mortality and severe neurologic deficits in neonates. The present work evaluated the preventative effect of photobiomodulation (PBM) preconditioning, and its underlying mechanism of action on brain damage in an HI model in neonatal rats. According to the optimal time response of ATP levels in brain samples removed from normal rats, a PBM preconditioning (PBM‐P) regimen (808 nm CW laser, 1 cm2 spot, 100 mW/cm2, 12 J/cm2) was delivered to the scalp 6 hours before HI. PBM‐P significantly attenuated cognitive impairment, volume shrinkage in the brain, neuron loss, dendritic and synaptic injury after HI. Further mechanistic investigation found that PBM‐P could restore HI‐induced mitochondrial dynamics and inhibit mitochondrial fragmentation, followed by a robust suppression of cytochrome c release, and prevention of neuronal apoptosis by inhibition of caspase activation. Our work suggests that PBM‐P can attenuate HI‐induced brain injury by maintaining mitochondrial dynamics and inhibiting the mitochondrial apoptotic pathway.  |
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| Keywords: | cognitive impairment hypoxia‐ischemia mitochondria neuroprotection photobiomodulation preconditioning |
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