Objective To investigate the effects and molecular mechanisms of ginsenoside Rg1 (GSRG1) on the proliferation, migration, and inflammatory cytokine expression of human gingival fibroblasts (HGFs) induced by lipopolysaccharide (LPS). Methods HGFs were isolated and cultured using the tissue block method. The effects of different concentrations of LPS (0, 1, 5, 10, 20 μg/mL) on inflammatory cytokines in HGFs were detected by ELISA. Cells were divided into three groups: control group (no treatment), LPS group (20 μg/mL LPS), and LPS+GSRG1 group (20 μg/mL LPS and 100 mg/L GSRG1). Cell proliferation was detected by cell counting kit-8 (CCK-8); cell migration was assessed by Transwell assay; intracellular reactive oxygen species (ROS) levels were compared using flow cytometry; and the expression levels of TNF-α, IL-6, NLRP3, p-p38, and p38 proteins were detected by Western blot. Results LPS concentrations of 5, 10, and 20 μg/mL significantly increased the expression of IL-6 and TNF-α in HGFs (P<0.05), with 20 μg/mL showing the strongest pro-inflammatory effect. Compared with the control group, there was no notable difference in the proliferation of HGFs in the LPS group at Day 1 and 2. However, on Day 3, 4 and 5, decreased cell proliferation, reduced migration, significantly increased ROS levels (P<0.001), elevated protein expression of TNF-α, IL-6, and NLRP3 (P<0.001), and reduced p-p38 protein expression (P<0.001) were exhibited. Compared with the LPS group, the LPS+GSRG1 group showed significantly enhanced cell proliferation and migration (P<0.05), reduced ROS levels, decreased protein expression of TNF-α, IL-6, and NLRP3, and increased p-p38 protein expression (P<0.001). There was no significant change in p38 expression among the three groups. Conclusion GSRG1 can alleviate the inhibitory effects of LPS on the proliferation and migration of HGFs and inhibit the inflammatory response, potentially through mechanisms involving p-p38 protein regulation.