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Signal transduction pathways involved in low intensity He–Ne laser‐induced respiratory burst in bovine neutrophils: A potential mechanism of low intensity laser biostimulation
Author(s) -
Duan Rui,
Liu Timon ChengYi,
Li Yan,
Guo Hong,
Yao LiBo
Publication year - 2001
Publication title -
lasers in surgery and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.888
H-Index - 112
eISSN - 1096-9101
pISSN - 0196-8092
DOI - 10.1002/lsm.1106
Subject(s) - calphostin c , protein kinase c , respiratory burst , signal transduction , phospholipase c , nadph oxidase , biology , microbiology and biotechnology , biochemistry , reactive oxygen species
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. Lasers Surg. Med. 29:174–178, 2001. © 2001 Wiley‐Liss, Inc.