Fig. 3

Anti-inflammatory mechanism of LIPUS on NS-SV-AC and NS-SV-DC cellular function. a Western blot analysis showed IκBα phosphorylation was obviously induced by TNF-α stimulation; however, when LIPUS treatment was administered following TNF-α treatment, IκBα, NF-κB, and IKKβ phosphorylation were inhibited. b Similar inhibitory effects of LIPUS were observed in IL-1β stimulation. c In Western blot analysis, IRAK1 was degraded after IL-1β stimulation, and LIPUS exposure failed to inhibit it. d The stimulation of both NS-SV-AC and NS-SV-DC cells with TNF-α or IL-1β resulted in a significant increase in levels of A20 mRNA, and A20 mRNA expression was further increased following treatment with LIPUS after TNF-α or IL-1β stimulation. *p < 0.05; **p < 0.01 (n = 6). A20 tumor necrosis factor-α-induced protein 3 (TNFAIP3), IKKβ inhibitor of nuclear factor κB kinase subunit β, IL-1β interleukin 1β, IRAK1 interleukin 1 receptor-associated kinase 1, IκBα inhibitor of nuclear factor of κ light polypeptide gene enhancer in B cells, α subunit, LIPUS low-intensity pulsed ultrasound, NF-κB nuclear factor κB, NS-SV-AC salivary gland acinar cells, NS-SV-DC salivary gland ductal cells, TNF-α tumor necrosis factor α