Signal transduction pathways involved in low intensity He-Ne laser-inducedrespiratory burst in bovine neutrophils: A potential mechanism of low intensity laser biostimulation

Citation
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
Citations number
31
Categorie Soggetti
Surgery
Journal title
LASERS IN SURGERY AND MEDICINE
ISSN journal
01968092 → ACNP
Volume
29
Issue
2
Year of publication
2001
Pages
174 - 178
Database
ISI
SICI code
0196-8092(2001)29:2<174:STPIIL>2.0.ZU;2-T
Abstract
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.