Objective: The aim of this study was to investigate the effect of therapeutic ultrasound (US) of cell viability and inflammatory cytokine in rat articular chondrocyte cultures stimulated with lipopolysaccharide (LPS). Design: One group pretest-posttest design. Methods: Cultured chondrocytes were treated with US and/or LPS and assessed for viability, Tumor necrosis factor (TNF)-α and Interleukin (IL)-1 production. Results: Oxidative stress was induced in rat chondrocytes with LPS. The cell viability was decreased in chondrocytes after treatment with LPS. The viability revealed that low-intensity pulsed ultrasound (LIPUS) exerted no significant cytotoxicity in the rat chondrocyte. LIPUS inhibited decreased cell viability in the presence of LPS (30 μg/ml) in a intensity dependent pattern at LIPUS (p＜0.05). TNF-α production in the presence of LPS was also inhibited in a dose dependent manner (p＜0.05 from 30 mW/cm2). IL-1 production in the presence of LPS was inhibited as well (p＜0.05 from 7.5 mW/cm2). Conclusions: Our results demonstrate that US was the anti-inflammatory effect of chondrocytes. LIPUS may exert its anti inflammatory effects through inhibition of TNF-α and IL-1 synthesis. These results suggest that US have potential for use as a pain relief and reduce the articular destruction.
Objective: The aim of this study was to investigate the effect of therapeutic ultrasound (US) of cell viability and inflammatory cytokine in rat articular chondrocyte cultures stimulated with lipopolysaccharide (LPS). Design: One group pretest-posttest design. Methods: Cultured chondrocytes were treated with US and/or LPS and assessed for viability, Tumor necrosis factor (TNF)-α and Interleukin (IL)-1 production. Results: Oxidative stress was induced in rat chondrocytes with LPS. The cell viability was decreased in chondrocytes after treatment with LPS. The viability revealed that low-intensity pulsed ultrasound (LIPUS) exerted no significant cytotoxicity in the rat chondrocyte. LIPUS inhibited decreased cell viability in the presence of LPS (30 μg/ml) in a intensity dependent pattern at LIPUS (p＜0.05). TNF-α production in the presence of LPS was also inhibited in a dose dependent manner (p＜0.05 from 30 mW/cm2). IL-1 production in the presence of LPS was inhibited as well (p＜0.05 from 7.5 mW/cm2). Conclusions: Our results demonstrate that US was the anti-inflammatory effect of chondrocytes. LIPUS may exert its anti inflammatory effects through inhibition of TNF-α and IL-1 synthesis. These results suggest that US have potential for use as a pain relief and reduce the articular destruction.
Introduction Methods Results Discussion
