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2025-01-01
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- IOC - Artigos de Periódicos [12341]
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LOW-LEVEL LASER THERAPY DECREASES LEVELS OF LUNG NEUTROPHILS ANTI-APOPTOTIC FACTORS BY A NF-KAPPAB DEPENDENT MECHANISM
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Universidade do Vale do Paraíba. Instituto de Pesquisa e Desenvolvimento. São José dos Campos, SP, Brasil.
Universidade do Vale do Paraíba. Instituto de Pesquisa e Desenvolvimento. São José dos Campos, SP, Brasil.
Universidade do Vale do Paraíba. Instituto de Pesquisa e Desenvolvimento. São José dos Campos, SP, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.
Universidade do Vale do Paraíba. Instituto de Pesquisa e Desenvolvimento. São José dos Campos, SP, Brasil.
Universidade do Vale do Paraíba. Instituto de Pesquisa e Desenvolvimento. São José dos Campos, SP, Brasil.
Universidade do Vale do Paraíba. Instituto de Pesquisa e Desenvolvimento. São José dos Campos, SP, Brasil.
Universidade do Vale do Paraíba. Instituto de Pesquisa e Desenvolvimento. São José dos Campos, SP, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.
Universidade do Vale do Paraíba. Instituto de Pesquisa e Desenvolvimento. São José dos Campos, SP, Brasil.
Universidade do Vale do Paraíba. Instituto de Pesquisa e Desenvolvimento. São José dos Campos, SP, Brasil.
Abstract
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/cm2. 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-κB 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 neutrophils
by an action mechanism in which the NF-κB seems to be involved.
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