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

✍ Scribed by Rui Duan; Timon Cheng-Yi Liu; Yan Li; Hong Guo; Li-Bo Yao

• Publisher: John Wiley and Sons
• Year: 2001
• Tongue: English
• Weight: 109 KB
• Volume: 29
• Category: Article
• ISSN: 0196-8092
• DOI: 10.1002/lsm.1106

✦ Synopsis

Abstract

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.