title: Low-level laser therapy associated to N-acetylcysteine lowers macrophage inflammatory protein-2 (MIP-2) mRNA expression and generation of intracellular reactive oxygen species in alveolar macrophages.
abstract: OBJECTIVE
  The aim of this work was to investigate the low-level laser therapy (LLLT) effect on alveolar macrophages (AM) activated by oxidative stress and lipopolysaccharide (LPS).
  
  
  BACKGROUND
  LLLT has been reported to actuate positively relieving the late and early symptoms of airway and lung inflammation. It is not known if the increased MIP-2 mRNA expression and intracellular reactive oxygen species (ROS) generation observed in acute lung inflammation (ALI) can be influenced by LLLT.
  
  
  METHODS
  Rat AM cell line (AMJ2-C11) was cultured with LPS or H(2)O(2) and laser irradiated. MIP-2 mRNA and ROS production in the AM were evaluated by Real Time-PCR and the 2',7'-dichlorofluorescin diacetate (DCFH-DA) respectively. The NF-κB protein in the AM was measured by the enzyme linked immunoassay method. To investigate the antioxidant effect of laser, the AM were prebathed with N-acetylcysteine (NAC) and then irradiated with laser. LLLT was also studied in the presence of an inhibitor of NF-κB (BMS 205820). In addition, the effect of LLLT on NF-κB protein was investigated.
  
  
  RESULTS
  LLLT attenuated the MIP-2 mRNA expression and intracellular ROS generation after LPS or H(2)O(2). When the AM were pretreated with NAC, the laser effect was potentiated. BMS 205820 suppresses the effect of LLLT on MIP-2 mRNA expression and ROS generation, stimulated by LPS or H(2)O(2). On NF-κB transcription factor, both the LLLT and NAC reduced this protein in the AM exposed to LPS or H(2)O(2). The synergistic effect between LLLT and NAC on the reduction the NF-κB was also evidenced.
  
  
  CONCLUSIONS
  Results indicate that there is a synergistic action of LLLT with NAC on MIP-2 mRNA expression from LPS- or H(2)O(2)-stimulated AM, and that both ROS intracellular generation and NF-kB signaling seem to be involved.
authors.affiliation: Institute of Research and Development, IP&D, UNIVAP, São José dos Campos, São Paulo, Brazil.
authors.forename: F Mafra
authors.initials: FM
authors.lastname: de Lima
authors.forename: A Balbin
authors.initials: AB
authors.lastname: Villaverde
authors.forename: R
authors.initials: R
authors.lastname: Albertini
authors.forename: A P Ligeiro
authors.initials: AP
authors.lastname: de Oliveira
authors.forename: H C Castro
authors.initials: HC
authors.lastname: Faria Neto
authors.forename: F
authors.initials: F
authors.lastname: Aimbire
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D000818:Animals; D002478:Cells, Cultured; D054426:Chemokine CXCL2 / Q000235:genetics* / Q000378:metabolism; D016166:Free Radical Scavengers / Q000494:pharmacology; D028022:Low-Level Light Therapy; D016676:Macrophages, Alveolar / Q000378:metabolism* / Q000528:radiation effects; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D054426:Chemokine CXCL2; C513296:Cxcl2 protein, rat; D016166:Free Radical Scavengers; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D000111:Acetylcysteine