Objective：We aimed to investigate the potential effects of low-intensity pulsed ultrasound（LIPUS）on the polarization and lipid droplet phagocytosis of macrophage，and further explore the underlying molecular mechanism. Methods：Murine tibial bone marrow was perfused to extract murine bone marrow-derived macrophage. Different intensities（4.825，19.300，43.425 mW/cm2）of LIPUS treatment were performed in macrophage. Then LPS was used to induce polarization of macrophage to the M1 phenotype. After that，we used flow cytometry and CCK-8 kit to determine the levels of apoptosis and viability of macrophage in different groups，respectively. Besides，the heating effects of LIPUS irradiation were measured by thermocouples. The mRNA expression of inflammatory-related genes was validated by q-PCR analysis. Western blot was conducted to explore the protein levels of NF-κB/MAPK pathway. Then，the phagocytosis of DiI-labeled OX-LDL was observed under inverted fluorescence microscope after 6 h co-culture with macrophage. Results：First，no significant difference of cell apoptosis in LIPUS group was shown in flow cytometry compared with that in the control group. The viability of macrophage examined in CCK-8 did not behave obvious difference. Besides，the results of temperature test demonstrated that the ultrasound conditions we set hardly changed the temperature of culture medium during LIPUS procedures. Then，results of q-PCR showed that mRNA levels of M1 phenotype genes were remarkedly up-regulated in LPS-induced macrophage compared with those in the control group，which was attenuated by LIPUS treatment（P < 0.05）. Moreover，LIPUS treatment down regulated LPS-induced phagocytosis of DiI-labeled OX-LDL（P < 0.05）. Results of western blot showed that LIPUS inhibited LPS-induced activation of NF-κB/MAPK pathways（P < 0.05）. Conclusion：Overall，our results demonstrated that LIPUS could reduce LPS-induced polarization of macrophage to the M1 phenotype，and phagocytosis of lipid droplet through inactivating NF-κB/MAPK pathway.