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

Abstract

Low-intensity pulsed ultrasound (US) has been reported to promote periodontal tissue regeneration and reduce inflammation in soft tissues and in bone infectious diseases. Here we investigated the effect of low-intensity pulsed US on the expression of lipopolysaccharide (LPS)-induced inflammatory factors in U937 macrophage cells. U937 cells were stimulated with different concentrations of LPS and exposed to different intensities of low-intensity pulsed US. Cell viability and apoptosis of U937 cells were determined by cell-counting kit assays and flow cytometry. A real-time polymerase chain reaction and an enzyme-linked immunosorbent assay were used to test the expression of inflammatory factors. The expression levels of toll-like receptor 4, p65, p-IκBα, and IκBα were assessed by western blots. Tumor necrosis factor α began to increase in U937 cells on induction with 1-μg/mL LPS. Low-intensity pulsed US at the intensity of 60 mW/cm2 was more effective in reducing interleukin 8 (IL-8) expression. Furthermore, LPS inhibited the viability and increased apoptosis of U937 cells, whereas low-intensity pulsed US significantly reversed these effects (P < .05). Low-intensity pulsed US reduced the protein expression of IL-6 and IL-8 at both gene and protein levels in U937 cells. The western blot and immunofluorescence showed that low-intensity pulsed US primarily suppressed the degradation and phosphorylation of IκBα and the translocation of p65 into the nuclei. Low-intensity pulsed US alleviated the expression of inflammatory factors induced by LPS in U937 cells. This process was modulated by suppressing the toll-like receptor 4-nuclear factor κB signaling pathway. Therefore, low-intensity pulsed US might be a potential immunomodulatory therapy for the treatment of periodontitis.