✦ LIBER ✦

In vivo effects of low level laser therapy on inducible nitric oxide synthase

✍ Scribed by Yumi Moriyama; Jacqueline Nguyen; Margarete Akens; Eduardo H. Moriyama; Lothar Lilge

Publisher: John Wiley and Sons
Year: 2009
Tongue: English
Weight: 140 KB
Volume: 41
Category: Article
ISSN: 0196-8092
DOI: 10.1002/lsm.20745

No coin nor oath required. For personal study only.

✦ Synopsis

Abstract

Background and Objective

Low level laser therapy (LLLT) has been demonstrated to modulate inflammatory processes with evidence suggesting that treatment protocol, such as wavelength, total energy, and number of treatments determine the clinical efficacy. In this study, the effects of LLLT mediated by different wavelengths and continuous versus pulsed delivery mode were quantified in a transgenic murine model with the luciferase gene under control of the inducible nitric oxide synthase (iNOS) expression.

Study Design/Materials and Methods

LLLT modulated iNOS gene expressed in the acute Zymosan‐induced inflammation model is quantified using transgenic mice (FVB/N‐Tg(iNOS‐luc)). Here an energy density of 5 J cm^−2^ at either 635, 660, 690, and 905 nm in continuous wave mode and at 905 nm for short pulse delivery were evaluated. Age of the animals was determined as additional modulating the inflammatory response and the LLLT efficacy for some treatment protocols.

Results

Animals younger than 15 weeks showed mostly reduction of iNOS expression, while older animals showed increased iNOS expression for some LLLT protocols. Intensity and time course of inducible nitric oxide expression was found to not only depend on wavelength, but also on the mode of delivery, continuous, or pulsed irradiation.

Conclusion

LLLT exhibit different effects in induced inflammatory process according to different wavelengths and wave mode. Upregulation of iNOS gene following 905 nm pulsed wave suggests a different mechanism in activating the inflammatory pathway response when compared to the continuous wave. Lasers Surg. Med. 41:227–231, 2009. © 2009 Wiley‐Liss, Inc.

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