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 data:
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.
Materials andMethods:
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.
Conclusion:
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.
