LED effectiveness for Inflammation, Pain & Oxidation

Have Pain, Inflammation or Oxidative Stress? Light Emitting Diodes again showing up as effective with oxidative stress, inflammation, pain and increases levels of one of the body’s most powerful natural antioxidant enzymes: superoxide dismutase (SOD). This study has dense language – bottom line the study for light emitting diodes: ” provides additional support for its use in the treatment of painful conditions of inflammatory” diseases.   Oxidative stress is a huge factor in many diseases and inflammation and pain are rampant issues in our society.

 

Neuroscience. 2016 Mar 18;324:485-495. doi: 10.1016/j.neuroscience.2016.03.035. [Epub ahead of print]
Light-emitting diode therapy reduces persistent inflammatory pain: Role of interleukin 10 and antioxidant enzymes.
Martins DF1, Turnes BL2, Cidral-Filho FJ3, Bobinski F4, Rosas RF5, Danielski LG6, Petronilho F6, Santos AR4.
Author information
Abstract
BACKGROUND:
During the last decades, the use of light-emitting diode therapy (LEDT) has increased significantly for the treatment of wound healing, analgesia and inflammatory processes. Nevertheless, scientific data on the mechanisms responsible for the therapeutic effect of LEDT are still insufficient. Thus, this study investigated the analgesic, anti-inflammatory and anti-oxidative effect of LEDT in the model of chronic inflammatory hyperalgesia.
EXPERIMENTAL PROCEDURES:
Mice injected with Complete Freund’s Adjuvant (CFA) underwent behavioral, i.e. mechanical and hot hyperalgesia; determination of cytokine levels (tumor necrosis factor-alpha (TNF-?), interleukin-1 beta (IL-1?), IL-10), oxidative stress markers (protein carbonyls and thiobarbituric acid reactive species (TBARS)) and antioxidant enzymes (catalase (CAT) and superoxide dismutase (SOD)). Additionally, mice were pretreated with either naloxone or fucoidin and mechanical hyperalgesia was assessed.
RESULTS:
LEDT inhibited mechanical and thermal hyperalgesia induced by CFA injection. LEDT did not reduce paw edema, neither influenced the levels of TNF-? and IL1-?; although it increased the levels of IL-10. LEDT significantly prevented TBARS increase in both acute and chronic phases post-CFA injection; whereas protein carbonyl levels were reduced only in the acute phase. LEDT induced an increase in both SOD and CAT activity, with effects observable in the acute but not in the chronic. And finally, pre-administration of naloxone or fucoidin prevented LEDT analgesic effect.
CONCLUSIONS:
These data contribute to the understanding of the neurobiological mechanisms involved in the therapeutic effect of LEDT as well as provides additional support for its use in the treatment of painful conditions of inflammatory etiology.
Copyright © 2016 IBRO. Published by Elsevier Ltd. All rights reserved.
KEYWORDS:
inflammation; low-level light therapy; mice; persistent pain
PMID: 27001179 [PubMed – as supplied by publisher]

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