Photobiomodulation Therapy Attenuates Hypoxic-Ischemic Injury in a Neonatal Rat Model

Lorelei Donovan Tucker, Yujiao Lu, Yan Dong, Luodan Yang, Yong Li, Ningjun Zhao, Quanguang Zhang

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Photobiomodulation (PBM) has been demonstrated as a neuroprotective strategy, but its effect on perinatal hypoxic-ischemic encephalopathy is still unknown. The current study was designed to shed light on the potential beneficial effect of PBM on neonatal brain injury induced by hypoxia ischemia (HI) in a rat model. Postnatal rats were subjected to hypoxic-ischemic insult, followed by a 7-day PBM treatment via a continuous wave diode laser with a wavelength of 808 nm. We demonstrated that PBM treatment significantly reduced HI-induced brain lesion in both the cortex and hippocampal CA1 subregions. Molecular studies indicated that PBM treatment profoundly restored mitochondrial dynamics by suppressing HI-induced mitochondrial fragmentation. Further investigation of mitochondrial function revealed that PBM treatment remarkably attenuated mitochondrial membrane collapse, accompanied with enhanced ATP synthesis in neonatal HI rats. In addition, PBM treatment led to robust inhibition of oxidative damage, manifested by significant reduction in the productions of 4-HNE, P-H2AX (S139), malondialdehyde (MDA), as well as protein carbonyls. Finally, PBM treatment suppressed the activation of mitochondria-dependent neuronal apoptosis in HI rats, as evidenced by decreased pro-apoptotic cascade 3/9 and TUNEL-positive neurons. Taken together, our findings demonstrated that PBM treatment contributed to a robust neuroprotection via the attenuation of mitochondrial dysfunction, oxidative stress, and final neuronal apoptosis in the neonatal HI brain.

Original languageEnglish (US)
Pages (from-to)514-526
Number of pages13
JournalJournal of Molecular Neuroscience
Volume65
Issue number4
DOIs
StatePublished - Aug 1 2018

Fingerprint

Brain Hypoxia-Ischemia
Wounds and Injuries
Ischemia
S 0139
Therapeutics
Mitochondrial Dynamics
Apoptosis
Semiconductor Lasers
In Situ Nick-End Labeling
Mitochondrial Membranes
Low-Level Light Therapy
Malondialdehyde
Brain Injuries
Mitochondria
Oxidative Stress
Lasers
Adenosine Triphosphate
Neurons
Hypoxia
Proteins

Keywords

  • Apoptosis
  • Mitochondrial dysfunction
  • Neonatal hypoxic-ischemia
  • Oxidative stress
  • Photobiomodulation therapy

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

Cite this

Photobiomodulation Therapy Attenuates Hypoxic-Ischemic Injury in a Neonatal Rat Model. / Tucker, Lorelei Donovan; Lu, Yujiao; Dong, Yan; Yang, Luodan; Li, Yong; Zhao, Ningjun; Zhang, Quanguang.

In: Journal of Molecular Neuroscience, Vol. 65, No. 4, 01.08.2018, p. 514-526.

Research output: Contribution to journalArticle

Tucker, Lorelei Donovan ; Lu, Yujiao ; Dong, Yan ; Yang, Luodan ; Li, Yong ; Zhao, Ningjun ; Zhang, Quanguang. / Photobiomodulation Therapy Attenuates Hypoxic-Ischemic Injury in a Neonatal Rat Model. In: Journal of Molecular Neuroscience. 2018 ; Vol. 65, No. 4. pp. 514-526.
@article{eebc98f2e9ee4ff1942bf791485032bd,
title = "Photobiomodulation Therapy Attenuates Hypoxic-Ischemic Injury in a Neonatal Rat Model",
abstract = "Photobiomodulation (PBM) has been demonstrated as a neuroprotective strategy, but its effect on perinatal hypoxic-ischemic encephalopathy is still unknown. The current study was designed to shed light on the potential beneficial effect of PBM on neonatal brain injury induced by hypoxia ischemia (HI) in a rat model. Postnatal rats were subjected to hypoxic-ischemic insult, followed by a 7-day PBM treatment via a continuous wave diode laser with a wavelength of 808 nm. We demonstrated that PBM treatment significantly reduced HI-induced brain lesion in both the cortex and hippocampal CA1 subregions. Molecular studies indicated that PBM treatment profoundly restored mitochondrial dynamics by suppressing HI-induced mitochondrial fragmentation. Further investigation of mitochondrial function revealed that PBM treatment remarkably attenuated mitochondrial membrane collapse, accompanied with enhanced ATP synthesis in neonatal HI rats. In addition, PBM treatment led to robust inhibition of oxidative damage, manifested by significant reduction in the productions of 4-HNE, P-H2AX (S139), malondialdehyde (MDA), as well as protein carbonyls. Finally, PBM treatment suppressed the activation of mitochondria-dependent neuronal apoptosis in HI rats, as evidenced by decreased pro-apoptotic cascade 3/9 and TUNEL-positive neurons. Taken together, our findings demonstrated that PBM treatment contributed to a robust neuroprotection via the attenuation of mitochondrial dysfunction, oxidative stress, and final neuronal apoptosis in the neonatal HI brain.",
keywords = "Apoptosis, Mitochondrial dysfunction, Neonatal hypoxic-ischemia, Oxidative stress, Photobiomodulation therapy",
author = "Tucker, {Lorelei Donovan} and Yujiao Lu and Yan Dong and Luodan Yang and Yong Li and Ningjun Zhao and Quanguang Zhang",
year = "2018",
month = "8",
day = "1",
doi = "10.1007/s12031-018-1121-3",
language = "English (US)",
volume = "65",
pages = "514--526",
journal = "Journal of Molecular Neuroscience",
issn = "0895-8696",
publisher = "Humana Press",
number = "4",

}

TY - JOUR

T1 - Photobiomodulation Therapy Attenuates Hypoxic-Ischemic Injury in a Neonatal Rat Model

AU - Tucker, Lorelei Donovan

AU - Lu, Yujiao

AU - Dong, Yan

AU - Yang, Luodan

AU - Li, Yong

AU - Zhao, Ningjun

AU - Zhang, Quanguang

PY - 2018/8/1

Y1 - 2018/8/1

N2 - Photobiomodulation (PBM) has been demonstrated as a neuroprotective strategy, but its effect on perinatal hypoxic-ischemic encephalopathy is still unknown. The current study was designed to shed light on the potential beneficial effect of PBM on neonatal brain injury induced by hypoxia ischemia (HI) in a rat model. Postnatal rats were subjected to hypoxic-ischemic insult, followed by a 7-day PBM treatment via a continuous wave diode laser with a wavelength of 808 nm. We demonstrated that PBM treatment significantly reduced HI-induced brain lesion in both the cortex and hippocampal CA1 subregions. Molecular studies indicated that PBM treatment profoundly restored mitochondrial dynamics by suppressing HI-induced mitochondrial fragmentation. Further investigation of mitochondrial function revealed that PBM treatment remarkably attenuated mitochondrial membrane collapse, accompanied with enhanced ATP synthesis in neonatal HI rats. In addition, PBM treatment led to robust inhibition of oxidative damage, manifested by significant reduction in the productions of 4-HNE, P-H2AX (S139), malondialdehyde (MDA), as well as protein carbonyls. Finally, PBM treatment suppressed the activation of mitochondria-dependent neuronal apoptosis in HI rats, as evidenced by decreased pro-apoptotic cascade 3/9 and TUNEL-positive neurons. Taken together, our findings demonstrated that PBM treatment contributed to a robust neuroprotection via the attenuation of mitochondrial dysfunction, oxidative stress, and final neuronal apoptosis in the neonatal HI brain.

AB - Photobiomodulation (PBM) has been demonstrated as a neuroprotective strategy, but its effect on perinatal hypoxic-ischemic encephalopathy is still unknown. The current study was designed to shed light on the potential beneficial effect of PBM on neonatal brain injury induced by hypoxia ischemia (HI) in a rat model. Postnatal rats were subjected to hypoxic-ischemic insult, followed by a 7-day PBM treatment via a continuous wave diode laser with a wavelength of 808 nm. We demonstrated that PBM treatment significantly reduced HI-induced brain lesion in both the cortex and hippocampal CA1 subregions. Molecular studies indicated that PBM treatment profoundly restored mitochondrial dynamics by suppressing HI-induced mitochondrial fragmentation. Further investigation of mitochondrial function revealed that PBM treatment remarkably attenuated mitochondrial membrane collapse, accompanied with enhanced ATP synthesis in neonatal HI rats. In addition, PBM treatment led to robust inhibition of oxidative damage, manifested by significant reduction in the productions of 4-HNE, P-H2AX (S139), malondialdehyde (MDA), as well as protein carbonyls. Finally, PBM treatment suppressed the activation of mitochondria-dependent neuronal apoptosis in HI rats, as evidenced by decreased pro-apoptotic cascade 3/9 and TUNEL-positive neurons. Taken together, our findings demonstrated that PBM treatment contributed to a robust neuroprotection via the attenuation of mitochondrial dysfunction, oxidative stress, and final neuronal apoptosis in the neonatal HI brain.

KW - Apoptosis

KW - Mitochondrial dysfunction

KW - Neonatal hypoxic-ischemia

KW - Oxidative stress

KW - Photobiomodulation therapy

UR - http://www.scopus.com/inward/record.url?scp=85050287858&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85050287858&partnerID=8YFLogxK

U2 - 10.1007/s12031-018-1121-3

DO - 10.1007/s12031-018-1121-3

M3 - Article

VL - 65

SP - 514

EP - 526

JO - Journal of Molecular Neuroscience

JF - Journal of Molecular Neuroscience

SN - 0895-8696

IS - 4

ER -