Photobiomodulation preconditioning prevents cognitive impairment in a neonatal rat model of hypoxia-ischemia

Luodan Yang; Yan Dong; Chongyun Wu; Yong Li; Yichen Guo; Baocheng Yang; Xuemei Zong; Michael R. Hamblin; Timon C.Y. Liu; Quanguang Zhang

doi:10.1002/jbio.201800359

Photobiomodulation preconditioning prevents cognitive impairment in a neonatal rat model of hypoxia-ischemia

Luodan Yang, Yan Dong, Chongyun Wu, Yong Li, Yichen Guo, Baocheng Yang, Xuemei Zong, Michael R. Hamblin, Timon C.Y. Liu, Quanguang Zhang

Neuroscience and Regenerative Medicine

Research output: Contribution to journal › Article › peer-review

33 Scopus citations

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.

Original language	English (US)
Article number	e201800359
Journal	Journal of Biophotonics
Volume	12
Issue number	6
DOIs	https://doi.org/10.1002/jbio.201800359
State	Published - Jun 2019

Keywords

cognitive impairment
hypoxia-ischemia
mitochondria
neuroprotection
photobiomodulation preconditioning

ASJC Scopus subject areas

General Chemistry
General Materials Science
General Biochemistry, Genetics and Molecular Biology
General Engineering
General Physics and Astronomy

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10.1002/jbio.201800359

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@article{b0cc881bfc0c4f81a97624df2d838530,

title = "Photobiomodulation preconditioning prevents cognitive impairment in a neonatal rat model of hypoxia-ischemia",

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.",

keywords = "cognitive impairment, hypoxia-ischemia, mitochondria, neuroprotection, photobiomodulation preconditioning",

author = "Luodan Yang and Yan Dong and Chongyun Wu and Yong Li and Yichen Guo and Baocheng Yang and Xuemei Zong and Hamblin, {Michael R.} and Liu, {Timon C.Y.} and Quanguang Zhang",

note = "Funding Information: This study was supported by Research Grant NS086929 from the National Institute of Neurological Disorders and Stroke, National Institutes of Health, USA, and National Natural Science Foundation Grant of China (61575065 to T.C.-Y.L.). M.R.H. was supported by US NIH grants R01AI050875 and R21AI121700. Funding Information: National Institutes of Health, Grant/Award Numbers: NS086929, R01AI050875, R21AI121700; National Natural Science Foundation of China, Grant/Award Number: 61575065 Funding Information: information National Institutes of Health, Grant/Award Number: NS086929, R01AI050875, R21AI121700; National Natural Science Foundation of China, Grant/Award Number: 61575065 This study was supported by Research Grant NS086929 from the National Institute of Neurological Disorders and Stroke, National Institutes of Health, USA, and National Natural Science Foundation Grant of China (61575065 to T.C.-Y.L.). M.R.H. was supported by US NIH grants R01AI050875 and R21AI121700. Publisher Copyright: {\textcopyright} 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim",

year = "2019",

month = jun,

doi = "10.1002/jbio.201800359",

language = "English (US)",

volume = "12",

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AU - Yang, Luodan

AU - Dong, Yan

AU - Wu, Chongyun

AU - Li, Yong

AU - Guo, Yichen

AU - Yang, Baocheng

AU - Zong, Xuemei

AU - Hamblin, Michael R.

AU - Liu, Timon C.Y.

AU - Zhang, Quanguang

N1 - Funding Information: This study was supported by Research Grant NS086929 from the National Institute of Neurological Disorders and Stroke, National Institutes of Health, USA, and National Natural Science Foundation Grant of China (61575065 to T.C.-Y.L.). M.R.H. was supported by US NIH grants R01AI050875 and R21AI121700. Funding Information: National Institutes of Health, Grant/Award Numbers: NS086929, R01AI050875, R21AI121700; National Natural Science Foundation of China, Grant/Award Number: 61575065 Funding Information: information National Institutes of Health, Grant/Award Number: NS086929, R01AI050875, R21AI121700; National Natural Science Foundation of China, Grant/Award Number: 61575065 This study was supported by Research Grant NS086929 from the National Institute of Neurological Disorders and Stroke, National Institutes of Health, USA, and National Natural Science Foundation Grant of China (61575065 to T.C.-Y.L.). M.R.H. was supported by US NIH grants R01AI050875 and R21AI121700. Publisher Copyright: © 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim

PY - 2019/6

Y1 - 2019/6

N2 - 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.

AB - 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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KW - mitochondria

KW - neuroprotection

KW - photobiomodulation preconditioning

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Photobiomodulation preconditioning prevents cognitive impairment in a neonatal rat model of hypoxia-ischemia

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Keywords

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