Inflammatory cytokines, interleukin (IL)‐1, IL‐6, and TNF‐α, are involved in inflammatory bone diseases such as rheumatoid osteoarthritis and periodontal disease. Particularly, periodontal disease, which destroys alveolar bone, is stimulated by lipopolysaccharide (LPS). Low‐intensity pulsed ultrasound (LIPUS) is used for bone healing in orthopedics and dental treatments. However, the mechanism underlying effects of LIPUS on LPS‐induced inflammatory cytokine are not well understood. We therefore aimed to investigate the role of LIPUS on LPS‐induced IL‐1α production. Mouse calvaria osteoblast‐like cells MC3T3‐E1 were incubated in the presence or absence of LPS (Porphyromonas gingivalis), and then stimulated with LIPUS for 30 min/day. To investigate the role of LIPUS, we determined the expression of IL‐1α stimulated with LIPUS and treated with an angiotensin II receptor type 1 (AT1) antagonist, Losartan. We also investigate to clarify the pathway of LIPUS, we transfected siRNA silencing AT1 (siAT1) in MC3T3‐E1. LIPUS inhibited mRNA and protein expression of LPS‐induced IL‐1α. LIPUS also reduced the nuclear translocation of NF‐κB by LPS‐induced IL‐1α. Losartan and siAT1 blocked all the stimulatory effects of LIPUS on IL‐1α production and IL‐1α‐mediated NF‐κB translocation induced by LPS. Furthermore, PLCβ inhibitor U73122 recovered NF‐κB translocation. These results suggest that LIPUS inhibits LPS‐induced IL‐1α via AT1‐PLCβ in osteoblasts. We exhibit that these findings are in part of the signaling pathway of LIPUS on the anti‐inflammatory effects of IL‐1α expression. LIPUS reduced IL‐1α production induced by LPS. LPS increased NF‐κB nuclear translocation. LIPUS stimulates AT1 receptor that acts inhibition of NF‐κB nuclear translocation.