Low-level laser therapy decreases levels of lung neutrophils anti-apoptotic factors by a NF-κB dependent mechanism

被引:41
作者
Aimbire, F. [1 ]
Santos, F. V. [1 ]
Albertini, R. [1 ]
Castro-Faria-Neto, H. C. [2 ]
Mittmann, J. [1 ]
Pacheco-Soares, C. [1 ]
机构
[1] Univ Vale Paraiba, Inst Res & Dev, BR-12240000 Sao Jose Dos Campos, SP, Brazil
[2] Fiocruz MS, Lab Immunopharmacol, BR-21045900 Rio De Janeiro, RJ, Brazil
关键词
lipopolysaccharide; diode 660 nm laser; lung inflammation; neutrophil anti-apoptotic; factors; NF-kappa B; LLLT;
D O I
10.1016/j.intimp.2007.12.007
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background and objective: Low-level laser therapy (LLLT) is a known modulator of inflammatory process. Herein we studied the effect of 660 nm diode laser on mRNA levels of neutrophils anti-apoptotic factors in lipopolysaccharide (LPS)-induced lung inflammation. Study design/ methodology: Mice were divided into 8 groups (n=7 for each group) and irradiated with energy dosage of 7.5 j/cm(2). The Bcl-xL and A1 mRNA levels in neutrophils were evaluated by Real Time-PCR (RT-PCR). The animals were irradiated after exposure time of LPS. Results: LLLT and an inhibitor of NF-kappa B nuclear translocation (BMS 205820) attenuated the mRNA levels of Bcl-xL and A1 mRNA in lung neutrophils obtained from mice subjected to LPS-induced inflammation. Conclusion: LLLT reduced the levels of anti-apoptotic factors in LPS inflamed mice lung neutro-phils by an action mechanism in which the NF-kappa B seems to be involved. (c) 2008 Published by Elsevier B.V.
引用
收藏
页码:603 / 605
页数:3
相关论文
共 7 条
[1]  
ABRAHAM E, 2000, AM J PHYSIOL, P279
[2]   Low level laser therapy partially restores trachea muscle relaxation response in rats with tumor necrosis factor α-mediated smooth airway muscle dysfunction [J].
Aimbire, F. ;
Bjordal, J. M. ;
Iversen, V. V. ;
Albertini, R. ;
Frigo, L. ;
Pacheco, M. T. T. ;
Castro-Faria-Neto, H. C. ;
Chavantes, M. C. ;
Labat, R. M. ;
Lopes-Martins, R. A. B. .
LASERS IN SURGERY AND MEDICINE, 2006, 38 (08) :773-778
[3]   Role of NF-κB in endotoxemia-induced alterations of lung neutrophil apoptosis [J].
Kupfner, JG ;
Arcaroli, JJ ;
Yum, HK ;
Nadler, SG ;
Yang, KY ;
Abraham, E .
JOURNAL OF IMMUNOLOGY, 2001, 167 (12) :7044-7051
[4]   NF-κB-mediated up-regulation of Bcl-x and Bfl-1/A1 is required for CD40 survival signaling in B lymphocytes [J].
Lee, HH ;
Dadgostar, H ;
Cheng, QW ;
Shu, JY ;
Cheng, GH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (16) :9136-9141
[5]   Nuclear factor-κB activates dual inhibition sites in the regulation of tumor necrosis factor-α-induced neutrophil apoptosis [J].
Niwa, M ;
Hara, A ;
Kanamori, Y ;
Hatakeyama, D ;
Saio, M ;
Takami, T ;
Matsuno, H ;
Kozawa, O ;
Uematsu, T .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2000, 407 (03) :211-219
[6]  
Parsey MV, 1998, J IMMUNOL, V160, P1007
[7]   Paediatric idiopathic inflammatory muscle disease - Recognition and management [J].
Pilkington, CA ;
Wedderburn, LR .
DRUGS, 2005, 65 (10) :1355-1365