Objective To investigate the influence and mechanism of chlorogenic acid (CGA) on autophagy induced by porphyromonas gingivalis (Pg) in human gingival epithelial cells (HGE). Methods HGE cells were cultured in vitro, and Pg was used to induce HGE cells to establish a cell model. Pg-induced HGE cells were treated with 5-60 mg/L CGA, respectively. Cell proliferation was detected by MTT assay, HGE cells were grouped into Control group, Pg group, CGA group (drug concentrations of 10.0, 20.0, 40.0 mg/L, respectively), and CGA+AMPK activator (AICAR) group (40.0 mg/L CGA+1.0 nmol/L AICAR), the apoptosis of HGE cells and the protein expressions of LC3Ⅱ, LC3I, Beclin-1, P62, p-ULK1, ULK1, p-AMPK and AMPK were detected respectively.Results CGA at 10-60 mg/L could greatly inhibit the proliferation of HGE cells induced by Pg. CGA at concentrations of 10.0, 20.0, and 40.0 mg/L were selected for subsequent experiments. Compared with the control group, the protein expression levels of LC3Ⅱ/I, Beclin-1, p-ULK1 and p-AMPK in the Pg group were greatly increased, and the expression level of P62 was greatly decreased (P<0.05); compared with the Pg group, the apoptosis rate of HGE cells treated with CGA at concentrations of 10.0, 20.0, and 40.0 mg/L was greatly increased (P<0.05), the protein expression levels of LC3Ⅱ/I, Beclin-1, p-ULK1, and p-AMPK were greatly decreased, and the expression level of P62 was greatly increased (P<0.05), which were drug concentration-dependent; AICAR could partially reverse the inhibitory effect of CGA on Pg-induced autophagy in HGE cells (P<0.05). Conclusion CGA inhibits Pg-induced autophagy of human gingival epithelial cells and promotes cell apoptosis by inhibiting the AMPK/ULK1 pathway