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光生物调节或低强度光疗的潜在机制。

Proposed Mechanisms of Photobiomodulation or Low-Level Light Therapy.

作者信息

de Freitas Lucas Freitas, Hamblin Michael R

机构信息

Programa de Pós-Graduação Interunidades Bioengenharia, University of São Paulo, São Carlos - SP, Brazil; Wellman Center for Photomedicine, Harvard Medical School, Boston, MA 02114, USA.

Wellman Center for Photomedicine, Harvard Medical School, Boston, MA 02114, USA; Department of Dermatology, Harvard Medical School, Boston, MA 02115, USA; Harvard-MIT Division of Health Sciences and Technology, Cambridge, MA 02139, USA.

出版信息

IEEE J Sel Top Quantum Electron. 2016 May-Jun;22(3). doi: 10.1109/JSTQE.2016.2561201.

DOI:10.1109/JSTQE.2016.2561201
PMID:28070154
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5215870/
Abstract

Photobiomodulation (PBM) also known as low-level laser (or light) therapy (LLLT), has been known for almost 50 years but still has not gained widespread acceptance, largely due to uncertainty about the molecular, cellular, and tissular mechanisms of action. However, in recent years, much knowledge has been gained in this area, which will be summarized in this review. One of the most important chromophores is cytochrome c oxidase (unit IV in the mitochondrial respiratory chain), which contains both heme and copper centers and absorbs light into the near-infra-red region. The leading hypothesis is that the photons dissociate inhibitory nitric oxide from the enzyme, leading to an increase in electron transport, mitochondrial membrane potential and ATP production. Another hypothesis concerns light-sensitive ion channels that can be activated allowing calcium to enter the cell. After the initial photon absorption events, numerous signaling pathways are activated via reactive oxygen species, cyclic AMP, NO and Ca2+, leading to activation of transcription factors. These transcription factors can lead to increased expression of genes related to protein synthesis, cell migration and proliferation, anti-inflammatory signaling, anti-apoptotic proteins, antioxidant enzymes. Stem cells and progenitor cells appear to be particularly susceptible to LLLT.

摘要

光生物调节作用(PBM),也被称为低强度激光(或光)疗法(LLLT),已为人所知近50年,但仍未得到广泛认可,这主要是由于其分子、细胞和组织作用机制尚不确定。然而,近年来,该领域已取得了很多知识,将在本综述中进行总结。最重要的发色团之一是细胞色素c氧化酶(线粒体呼吸链中的第四单元),它同时含有血红素和铜中心,并吸收近红外区域的光。主要假说是光子使抑制性一氧化氮从该酶上解离,导致电子传递、线粒体膜电位和ATP生成增加。另一个假说涉及可被激活从而使钙进入细胞的光敏感离子通道。在最初的光子吸收事件之后,众多信号通路通过活性氧、环磷酸腺苷、一氧化氮和钙离子被激活,导致转录因子的激活。这些转录因子可导致与蛋白质合成、细胞迁移和增殖、抗炎信号传导、抗凋亡蛋白、抗氧化酶相关的基因表达增加。干细胞和祖细胞似乎对低强度激光疗法尤为敏感。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ace/5215870/fb6dfcee2b2f/nihms797827f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ace/5215870/72eb88113140/nihms797827f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ace/5215870/f32482c60989/nihms797827f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ace/5215870/657e21d091fe/nihms797827f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ace/5215870/ce5a68b03eb0/nihms797827f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ace/5215870/fb6dfcee2b2f/nihms797827f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ace/5215870/72eb88113140/nihms797827f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ace/5215870/f32482c60989/nihms797827f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ace/5215870/657e21d091fe/nihms797827f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ace/5215870/ce5a68b03eb0/nihms797827f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ace/5215870/fb6dfcee2b2f/nihms797827f5.jpg

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