title: Near infrared radiation rescues mitochondrial dysfunction in cortical neurons after oxygen-glucose deprivation.
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.
authors.affiliation: Departments of Neurology and Radiology, Neuroprotection Research Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, 02129, USA, Yu.Zhanyang@mgh.harvard.edu.
authors.forename: Zhanyang
authors.initials: Z
authors.lastname: Yu
authors.forename: Ning
authors.initials: N
authors.lastname: Liu
authors.forename: Jianhua
authors.initials: J
authors.lastname: Zhao
authors.forename: Yadan
authors.initials: Y
authors.lastname: Li
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: McCarthy
authors.forename: Clark E
authors.initials: CE
authors.lastname: Tedford
authors.forename: Eng H
authors.initials: EH
authors.lastname: Lo
authors.forename: Xiaoying
authors.initials: X
authors.lastname: Wang
mesh_terms: D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D016923:Cell Death / Q000528:radiation effects; D002540:Cerebral Cortex / Q000166:cytology / Q000528:radiation effects*; D005260:Female; D005947:Glucose / Q000172:deficiency*; D002534:Hypoxia, Brain / Q000532:radiotherapy*; D007259:Infrared Rays / Q000627:therapeutic use*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000528:radiation effects; D051379:Mice; D008810:Mice, Inbred C57BL; D028361:Mitochondrial Diseases / Q000532:radiotherapy*; D009474:Neurons / Q000528:radiation effects*; D061251:Primary Cell Culture; D013778:Tetrazolium Salts; D013844:Thiazoles
chemical_list: D013778:Tetrazolium Salts; D013844:Thiazoles; D000255:Adenosine Triphosphate; D007770:L-Lactate Dehydrogenase; C022616:thiazolyl blue; D005947:Glucose