Dracorhodin quickly and accurately affects the proliferation of scar fibroblasts at any type of cell cycle distribution. Hypertrophic scar fibroblasts (FB) are proliferative cells, with a short G1 phase duration while showing a high proportion of active DNA synthesis in the S and G2 phases. Currently, it is known that there exist DNA damage checkpoints in the cell cycle, including the detection point before DNA replication in G1 phase and the G2/M checkpoint during mitosis. Their function is to arrest cells at these checkpoints when DNA damage or mutation occurs, allowing for DNA repair. If the repair fails, the cells undergo apoptosis. Our results show that Dracorhodin (Dp) decreases the proliferation index of FB in a time- and dose-dependent manner and induces FB apoptosis. The time effect seems more pronounced. For 0 (control), 20, 40, 80 mg/L Dp-treated FB over 24 hours, as the dose increases, the number of cells in the G1 phase increases, while the content of cells in the S and G2 phases gradually decreases. This indicates that Dp can block FB transition from G1 to S phase, causing cell cycle arrest in G1 phase, thereby inhibiting cell proliferation. Thus, Dp inhibits the growth of scar FB proliferation by regulating the cell cycle and inducing apoptosis. Information about the specific mechanism by which Dp induces FB apoptosis remains to be studied further.