Objective To investigate the therapeutic effect and mechanism of asmall-molecule activator of ULK1 in the treatment of Parkinson’s disease （PD） by inducing cytoprotective autophagy.Methods MPP⁺ was used to establish in vitro PD model cells， and then the model cells were treated with different concentrations of BL918， a small-molecule activator of ULK1， to observe the effect of BL918 on the viability and apoptosis of PD model cells. Western blotting was used to investigate the effect of BL918 on the expression of the autophagy-specific proteins P62 and LC3 II in the PD cell models， and the autophagy inhibitor 3MA was used to analyze its inhibitory effect on autophagy induced by MPP⁺ and BL918.Results With the increase in MPP⁺ concentration， the viability of the PD model cells tended to decrease gradually， while the viability of cells was improved after BL918 intervention. With the increase inthe concentration of BL918 intervention， the viability of PD model cells increased and reached the peak at the concentration of 0.5 mM， which was significantly higher than the viability of cells at other concentrations （P<0.05）. Flow cytometry showed that BL918 intervention effectively reduced the apoptosis of PD model cells， with asignificantly lower apoptosis rate than the PD model group （P<0.05）. Western blotting showed that the application of BL918 increased the protein expression of P62 and LC3 II （P<0.05）. After intervention with the autophagy inhibitor 3MA， the tendency of BL918 to reduce the apoptosis of PD model cells was weakened.Conclusions The small-molecule activator of ULK1 has a good protective effect on PD model cells established by MPP⁺ and can significantly reduce the apoptosis of PD cells， since ULK1 can induce protective autophagy in cells.