Low energy laser light (632.8 nm) suppresses amyloid-β peptide-induced oxidative and inflammatory responses in astrocytes

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dc.contributor.authorYang, Xiaoguang
dc.contributor.authorAskarova, Sholpan
dc.contributor.authorSheng, Wenwen
dc.contributor.authorChen, JK
dc.contributor.authorSun, Albert Y.
dc.contributor.authorSun, Grace Y.
dc.contributor.authorYao, Gang
dc.contributor.authorLeea, James C-M.
dc.date.accessioned2016-02-08T06:21:54Z
dc.date.available2016-02-08T06:21:54Z
dc.date.issued2010-09-25
dc.description.abstractOxidative stress and inflammation are important processes in the progression of Alzheimer's disease (AD). Recent studies have implicated the role of amyloid β-peptides (Aβ) in mediating these processes. In astrocytes, oligomeric Aβ induces the assembly of NADPH oxidase complexes resulting in its activation to produce anionic superoxide. Aβ also promotes production of pro-inflammatory factors in astrocytes. Since low energy laser has previously been reported to attenuate oxidative stress and inflammation in biological systems, the objective of this study was to examine whether this type of laser light was able to abrogate the oxidative and inflammatory responses induced by Aβ. Primary rat astrocytes were exposed to Helium-Neon laser (λ=632.8 nm), followed by the treatment with oligomeric Aβ. Primary rat astrocytes were used to measure Aβ-induced production of superoxide anions using fluorescence microscopy of dihydroethidium (DHE), assembly of NADPH oxidase subunits by the colocalization between the cytosolic p47phox subunit and the membrane gp91phox subunit using fluorescent confocal microscopy, phosphorylation of cytosolic phospholipase A2 (cPLA2), and expressions of pro-inflammatory factors including interleukin-1β (IL-1β) and inducible nitric-oxide synthase (iNOS) using Western blot Analysis. Our data showed that laser light at 632.8 nm suppressed Aβ-induced superoxide production, colocalization between NADPH oxidase gp91phox and p47phox subunits, phosphorylation of cPLA2, and the expressions of IL-1β and iNOS in primary astrocytes. We demonstrated for the first time that 632.8 nm laser was capable of suppressing cellular pathways of oxidative stress and inflammatory responses critical in the pathogenesis in AD. This study should prove to provide the groundwork for further investigations for the potential use of laser therapy as a treatment for AD.ru_RU
dc.identifier.urihttp://nur.nu.edu.kz/handle/123456789/1177
dc.language.isoenru_RU
dc.publisherUS National Library of Medicine National Institutes of Healthru_RU
dc.rightsAttribution-NonCommercial-ShareAlike 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/us/*
dc.subjectphospholipase A2ru_RU
dc.subjectinterleukin-1βru_RU
dc.subjectiNOSru_RU
dc.subjectNADPH oxidaseru_RU
dc.subjectoxidative stressru_RU
dc.subjectphosphorylationru_RU
dc.subjectinflammationru_RU
dc.titleLow energy laser light (632.8 nm) suppresses amyloid-β peptide-induced oxidative and inflammatory responses in astrocytesru_RU
dc.typeArticleru_RU

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