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

Objectives 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. Methods 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. Results 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/cm 2 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. Conclusions 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.