Objective: This study aims to verify the anti-inflammatory effect of baicalin in an inflammatory environment and explore its influence on the odontogenic/osteogenic differentiation of human dental pulp stem cells (hDPSCs), providing a reference for the treatment of pulpitis. Methods: Select early inflammatory dental pulp tissue from humans to make frozen sections and perform HE staining and IL-1β immunohistochemical staining. Human monocyte leukemia cells (THP-1) were differentiated into macrophages and polarized to the M1 subtype under the induction of lipopolysaccharide (LPS) and interferon-γ (IFN-γ). Then, baicalin (50 μM) was used for treatment. The expression levels of INOS, IL-1β, and IL-8 were analyzed using immunofluorescence, real-time quantitative PCR (RT-qPCR), and Western blot. Additionally, the expression changes of LC3B, Beclin-1, and P62 were assessed by Western blot to monitor autophagic flux alterations in macrophages. To further investigate the relationship between inflammation inhibition and autophagy, we employed the autophagy inhibitor 3-MA to block autophagic flux and re-evaluated the expression changes of IL-1β and IL-8. Supernatants from macrophages treated under various conditions were collected, and the conditioned medium was prepared to act on human dental pulp stem cells. The odontogenic/osteogenic differentiation ability of hDPSCs in an inflammatory environment was analyzed by ALP staining, alizarin red (ARS) staining, RT-PCR, and Western blot. Results: The expression of IL-1β around the inflamed area of early pulpitis tissue was significantly increased. After LPS and IFN-γ induced THP-1, THP-1 macrophages polarized from M0 to M1, and the expressions of INOS, IL-1β and IL-8 significantly increased. After co-incubation with 50μM BA for 24 hours, the polarization degree of M1 macrophages significantly decreased, the mRNA levels of IL-1β and IL-8 significantly decreased, while the expression level of IL-6 showed no statistical difference compared with the M1 group. After adding the supernatant of M1 macrophages to hDPSCs and inducing mineralization for 7~21 days, the alkaline phosphatase activity of hDPSCs decreased, the calcium salt deposition significantly reduced, and the expressions of ALP, DSPP, RUNX2, OPN and COL-1 significantly decreased. When adding the supernatant of M1 macrophages treated with BA, the alkaline phosphatase activity of hDPSCs significantly increased, the calcium salt deposition significantly increased, and the expressions of ALP, DSPP, RUNX2, OPN and COL-1 significantly increased. Conclusion: Baicalin can inhibit inflammatory responses by activating autophagy, thereby enabling hDPSCs to function in an inflammatory microenvironment.