Signal transduction pathways involved in low intensity He-Ne laser-inducedrespiratory burst in bovine neutrophils: A potential mechanism of low intensity laser biostimulation
R. Duan et al., Signal transduction pathways involved in low intensity He-Ne laser-inducedrespiratory burst in bovine neutrophils: A potential mechanism of low intensity laser biostimulation, LASER SURG, 29(2), 2001, pp. 174-178
Background and Objective: Low intensity He-Ne laser irradiation has been re
ported to induce respiratory burst of neutrophils for a long time, but the
mechanism remains obscure. We speculated that it is mediated by some signal
transduction pathways.
Study Design/Materials and Methods: The protein tyrosine kinases (PTKs) inh
ibitor, genistein, the phospholipase C (PLC) inhibitor, U-73122, and the pr
otein kinase C (PKC) inhibitor, calphostin C, were used to probe signal tra
nsduction pathways of respiratory burst of bovine neutrophils which were in
duced by He-Ne laser at a dose of 300 J/m(2), respectively.
Results: The inhibitor of PTKs can completely inhibit the He-Ne laser-induc
ed respiratory burst of neutrophils. PLO and PKC inhibitors can obviously r
educe it, but not fully inhibit it.
Conclusion: These results suggest that PTKs play a key role in the He-Ne la
ser-induced respiratory burst of neutrophils and [PTK-PLC-PKC-NADPH oxidase
] signal transduction pathways may be involved in this process. (C) 2001 Wi
ley-Liss, Inc.