Signal transduction pathways involved in low intensity He-Ne laser-induced respiratory burst in bovine neutrophils: a potential mechanism of low intensity laser biostimulation.
BACKGROUND AND OBJECTIVE: Low intensity He-Ne laser irradiation has been reported 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) inhibitor, genistein, the phospholipase C (PLC) inhibitor, U-73122, and the protein kinase C (PKC) inhibitor, calphostin C, were used to probe signal transduction pathways of respiratory burst of bovine neutrophils which were induced 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-induced respiratory burst of neutrophils. PLC and PKC inhibitors can obviously reduce it, but not fully inhibit it. CONCLUSION: These results suggest that PTKs play a key role in the He-Ne laser-induced respiratory burst of neutrophils and [PTK-PLC-PKC-NADPH oxidase] signal transduction pathways may be involved in this process.