Radial shock waves effectively introduced NF‐kappa B decoy into rat achilles tendon cells in vitro

Abstract

The purpose of this study was to test if radial shock waves could enhance the introduction of nuclear factor-kappa B (NF-kB) decoy oligodeoxynucleotides, which is reported to markedly inhibit NF-kB activation and suppress pro-inflammatory cytokine gene expression, using rat Achilles tendon cells. In the presence of NF-kB decoy labeled with or without fluorescein isothiocyanate (FITC) in culture media, radial shock waves were applied to the tendon cells in variable conditions and cultivated for 24 h. The transfection rate was assessed by counting FITC-positive cells, and IL-1-induced NF-kB activation in the cells was assessed. Radial shock waves significantly enhanced introduction of NF-kB decoy-FITC into the tendon cells. IL-1-induced NF-kB activation was significantly inhibited by pretreatment of the cells with NF-kB decoy combined with radial shock wave exposure. The present study demonstrated the effectiveness of radial shock waves on introduction of NF-kB decoy into tendon cells. Radial shock wave treatment combined with local NF-kB decoy administration could be a novel therapeutic strategy for chronic tendinopathy. ß

Application of extracorporeal shock wave therapy in nervous system diseases: A review

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Inhibitory Effect of Low‐Intensity Pulsed Ultrasound on the Expression of Lipopolysaccharide‐Induced Inflammatory Factors in U937 Cells

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“…36,40 Some researchers believe that TLR4-NF-jB signaling may be a therapeutic target for treatments. [41][42][43] Shen et al 26 investigated the effect of selenomethionine on LPS-induced inflammatory responses and found inhibition of TNF-a and cyclooxygenase 2 expression with selenomethionine treatment. Furthermore, selenomethionine alleviated the degradation of IjBa and the translocation of p50.…”

The roles and mechanisms of the NF-κB signaling pathway in tendon disorders

“…The NF-κB signaling pathway has been regarded as a typical proinflammatory signal transduction pathway, the activation of which is involved in the regulation of multiple genes, including proinflammatory cytokines, chemokines, adhesion molecules, and enzymes (17,18). It has been reported that blocking the activation of NF-κB signaling pathway in tendon disorders has been more effective than completely inhibiting all the inflammatory response (19)(20)(21). Nevertheless, there is currently insufficient mechanistic understanding of the NF-κB signaling pathway in tendon disorders to manifest this possibility in practice.…”