Effect And Mechanism Of Low-level Laser Irradiation On Rat Dorsal Root Ganglion Neurons And Chondrocytes

Nitric oxide (NO) and Ca2+ are important signaling molecules involved in pain transmission. The self-renewal capacity of injured-cartilage is very limited, and there is no ideal treatment in clinic so far to date. Based on the confocal microscopy imaging and biological methods, effect of low-level laser irradiation (LLLI) on NO release and effect of adenosine receptors on LLLI-induced Ca2+ changes in dorsal root ganglion neurons (DRG) neurons were performed in order to explore the cellular and molecular mechanism of pain relief by LLLI. And the effect of LLLI on the growth of cultured chondrocytes was also performed in this study aiming for exploring the cellular and molecular mechanism of cartilage repair by LLLI. These results showed:1. LLLI could promote NO release in a wavelength-and dose-correlated manner in Ca2+-free condition. And the photochemical mechanism and the activity of nitric oxide synthesis (NOS) were involved in the rising NO release induced by LLLI.2. Adenosine could modulate intracellular Ca2+release in DRG neurons through adenosine A1 receptor (A1R) and adenosine A3 receptor (A3R). LLLI could increase intracellular Ca2+ release in DRG neurons in a wavelength- and dose- correlated manner. A1R and A3R could block the LLLI induced Ca+ increase.3. LLLI could stimulate chondrocytes proliferation as well as secretion of collagen type II and glycosaminoglycans in the condition of 2% fetal bovine serum (FBS) and 5% FBS in a wavelength- and dose-correlated manner.These results suggest that one of the mechanisms of LLLT of relieving pain might be that LLLI firstly modulating the NO and adenosine and then influencing intracellular Ca2+ release in the DRG neurons. The present results demonstrate that LLLI may be used to treat OA, not only relieving pain but also stimulating the articular chondrocytes growth to repair the injured articular cartilage in OA.