To investigate the mechanism of Shenbai Granules(SBG) in intervening in the pyroptosis pathway to reduce inflammation in human gastric mucosal epithelial cells(GES-1).Methods:The inflammation model was established in GES-1 cells by lipopolysaccharide(LPS) induction.Different concentrations of LPS were used to treat GES-1 cells，and Western blot(WB) was employed to detect the expression of NOD-like receptor protein 3(NLRP3) to determine the optimal concentration for LPS-induced model establishment.GES-1 cells were treated with different concentrations of SBG，and the Cell Counting Kit-8(CCK-8) assay was used to verify the cytotoxicity of SBG and select the optimal intervention concentration.The following groups were set up in this study：blank group，model group，and SBG group.Except for the blank group，the other two groups were treated with LPS to establish the inflammation model.After 24 hours of intervention，WB was used to detect the expression of NLRP3，Caspase-1，Cleaved Caspase-1，Gasdermin D(GSDMD)，and Cleaved GSDMD.Flow cytometry was used to measure reactive oxygen species(ROS) levels and pyroptosis rate.Enzyme-linked immunosorbent assay(ELISA) was used to detect the levels of interleukin-18(IL-18)，interleukin-1β(IL-1β)，and tumor necrosis factor-α(TNF-α) in the cell supernatant.Results:The optimal concentration for the LPS-induced model was 0.5 μg/mL.CCK-8 assay revealed that SBG did not exhibit cytotoxic effects on GES-1 cells.Compared with the blank group，the model group showed increased expression of NLRP3，Caspase-1，Cleaved Caspase-1，GSDMD，Cleaved GSDMD，ROS，and pyroptosis rate.In contrast，compared to the model group，the SBG group exhibited significantly reduced expression of the above indicators(all P<0.05).Conclusion:SBG can inhibit the pyroptosis pathway to reduce LPS-induced inflammation and oxidative stress in GES-1 cells，and alleviate pyroptosis.