Keratinocyte proliferation delay was a prominent clinical manifestation of diabetes, significantly impeding the wound healing process in diabetic mice. The potential therapeutic role of (−)-epigallocatechin gallate (EGCG) has been recognized due to its ability to enhance wound healing under diabetic conditions, but the underlying mechanism remained unclear. This study elucidates that EGCG expedited wound healing in diabetic mice by accelerating re-epithelialization and collagen deposition. Remarkably, we observed that EGCG promotes epidermal cell proliferation and enhances wound healing process in diabetic mice. We also discovered an overexpression of the Notch pathway in the epidermal cells of diabetic mice. Interestingly, EGCG effectively suppresses this overexpressed Notch pathway, suggesting a targeted mechanism for its therapeutic effects. Furthermore, the experiments with human immortalized keratinocytes (HaCaT) confirmed that high glucose levels activated the Notch signaling pathway, which was subsequently inhibited by EGCG treatment. In conclusion, our study reveals that EGCG improves wound healing in streptozotocin (STZ)-induced diabetic mice by targeting the Notch pathway in epidermal cells. These findings offered novel insights into therapeutic strategies for diabetic wounds and highlight EGCG as a promising candidate for treating chronic wounds.