Abstract： Objective:To discuss the effect of hyperbaric oxygen（HBO）combined with catechin（Can）on lipopolysaccharide（LPS）-induced inflammatory response of human bone marrow stromal HS-5 cells and its mechanism of action.Methods:A portion of normal HS-5 cells in good condition were assigned as control group（DMEM medium），and another portion of HS-5 cells were used to establish the bone marrow inflammatory cell model induced by LPS which were then divided into four groups for different interventions：the model group（1.0 μg/ml LPS was added into the medium），the HBO group（1.0 μg/ml LPS was added into the medium and then treated with 0.2 MPa HBO），the Can group（1.0 μg/ml LPS and 150 μmol/L Can were added into the medium）and the combined group（1.0 μg/ml LPS and 150 μmol/L Can were added into the medium and then treated with 0.2 MPa HBO）. The proliferation of HS-5 cells in each group was detected by the CCK-8 method，and the expression levels of IL-1β，IL-6，TNF-α，and IL-10 in HS-5 inflammatory cell fluid were measured by ELISA. The apoptosis of HS-5 inflammatory cells in each group was detected by flow cytometry，and the expression levels of TLR6/NF-κB signaling pathway proteins in HS-5 inflammatory cells were detected by western blotting.Results:The results of the CCK-8 method showed that Can at the concentration of 150 μmol/L inhibited the proliferation of HS-5 cells induced by LPS at 1.0 μg/ml，which was used as a reference to establish an inflammatory cell model of bone marrow HS-5. The results of flow cytometry showed that the survival rate of HS-5 inflammatory cells in the combined group［（13.99±1.25）%］was significantly lower than that in the model group［（46.69±4.27）%］，the HBO group［（39.28±3.74）%］，and the Can group［（23.14±2.20）%］，with statistically significant differences（ P<0.05 or P<0.01）. Compared with the model group，the HBO group，and the Can group，the expression levels of proteins（TLR6 and p-NF-κB）in HS-5 inflammatory cells in the combined group were significantly decreased（ P<0.01）. Conclusion:Can combine with HBO has a strong anti-inflammatory effect on HS-5 inflammatory cells，and its possible mechanism of action is to inhibit LPS-induced bone marrow inflammatory response by regulating the TLR6/NF-κB signaling pathway，which can provide new ideas for the treatment of bone injuries.