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2015 ; 30
(2
): 491-6
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Near infrared radiation rescues mitochondrial dysfunction in cortical neurons
after oxygen-glucose deprivation
#MMPMID24599760
Yu Z
; Liu N
; Zhao J
; Li Y
; McCarthy TJ
; Tedford CE
; Lo EH
; Wang X
Metab Brain Dis
2015[Apr]; 30
(2
): 491-6
PMID24599760
show ga
Near infrared radiation (NIR) is known to penetrate and affect biological systems
in multiple ways. Recently, a series of experimental studies suggested that low
intensity NIR may protect neuronal cells against a wide range of insults that
mimic diseases such as stroke, brain trauma and neurodegeneration. However, the
potential molecular mechanisms of neuroprotection with NIR remain poorly defined.
In this study, we tested the hypothesis that low intensity NIR may attenuate
hypoxia/ischemia-induced mitochondrial dysfunction in neurons. Primary cortical
mouse neuronal cultures were subjected to 4 h oxygen-glucose deprivation followed
by reoxygenation for 2 h, neurons were then treated with a 2 min exposure to
810-nm NIR. Mitochondrial function markers including MTT reduction and
mitochondria membrane potential were measured at 2 h after treatment.
Neurotoxicity was quantified 20 h later. Our results showed that 4 h
oxygen-glucose deprivation plus 20 h reoxygenation caused 33.8?±?3.4 % of neuron
death, while NIR exposure significantly reduced neuronal death to 23.6?±?2.9 %.
MTT reduction rate was reduced to 75.9?±?2.7 % by oxygen-glucose deprivation
compared to normoxic controls, but NIR exposure significantly rescued MTT
reduction to 87.6?±?4.5 %. Furthermore, after oxygen-glucose deprivation,
mitochondria membrane potential was reduced to 48.9?±?4.39 % of normoxic control,
while NIR exposure significantly ameliorated this reduction to 89.6?±?13.9 % of
normoxic control. Finally, NIR significantly rescued OGD-induced ATP production
decline at 20 min after NIR. These findings suggest that low intensity NIR can
protect neurons against oxygen-glucose deprivation by rescuing mitochondrial
function and restoring neuronal energetics.
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