Here, we show that extracorporeal shock waves (ESW), at a low energy density value, quickly increase neuronal nitric oxide synthase (nNOS) activity and basal nitric oxide (NO) production in the rat glioma cell line C6. In addition, the treatment of C6 cells with ESW reverts the decrease of nNOS activity and NO production induced by a mixture of lipopolysaccharides (LPS), interferon-γ (IFN-γ) plus tumour necrosis factor-α (TNF-α). Finally, ESW treatment efficiently downregulates NF-κB activation and NF-κB-dependent gene expression, including inducible NOS and TNF-α. The present report suggests a possible molecular mechanism of the anti-inflammatory action of ESW treatment.
Ciampa, A.r., DE PRATI, A.c., Amelio, E., Cavalieri, E., Persichini, T., Colasanti, M., et al. (2005). Nitric oxide mediates anti-inflammatory action of extracorporeal shock waves. FEBS LETTERS, 579, 6839-6845 [10.1016/j.febslet.2005.11.023].
Nitric oxide mediates anti-inflammatory action of extracorporeal shock waves
PERSICHINI, TIZIANA;
2005-01-01
Abstract
Here, we show that extracorporeal shock waves (ESW), at a low energy density value, quickly increase neuronal nitric oxide synthase (nNOS) activity and basal nitric oxide (NO) production in the rat glioma cell line C6. In addition, the treatment of C6 cells with ESW reverts the decrease of nNOS activity and NO production induced by a mixture of lipopolysaccharides (LPS), interferon-γ (IFN-γ) plus tumour necrosis factor-α (TNF-α). Finally, ESW treatment efficiently downregulates NF-κB activation and NF-κB-dependent gene expression, including inducible NOS and TNF-α. The present report suggests a possible molecular mechanism of the anti-inflammatory action of ESW treatment.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
