Abstract:
: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.
journal_name
Metab Brain Disjournal_title
Metabolic brain diseaseauthors
Yu Z,Liu N,Zhao J,Li Y,McCarthy TJ,Tedford CE,Lo EH,Wang Xdoi
10.1007/s11011-014-9515-6subject
Has Abstractpub_date
2015-04-01 00:00:00pages
491-6issue
2eissn
0885-7490issn
1573-7365journal_volume
30pub_type
杂志文章abstract::There is substantial clinical and experimental evidence that ammonia is a major factor in the pathogenesis of hepatic encephalopathy. In the article is demonstrated that in hepatocellular dysfunction, ammonia detoxification to glutamine (GLN) in skeletal muscle, brain, and likely the lungs, is activated. In addition t...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
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journal_title:Metabolic brain disease
pub_type: 临床试验,杂志文章
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journal_title:Metabolic brain disease
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doi:10.1007/s11011-005-2476-z
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journal_title:Metabolic brain disease
pub_type: 杂志文章,meta分析
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journal_title:Metabolic brain disease
pub_type: 临床试验,杂志文章
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journal_title:Metabolic brain disease
pub_type: 杂志文章
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-017-9988-1
更新日期:2017-08-01 00:00:00
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journal_title:Metabolic brain disease
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