This study investigated the pathological and molecular effects of Centella asiatica extract–based cream and ointment formulations on burn wound healing in streptozotocin-induced diabetic rats. A total of 92 female Wistar albino rats were assigned to six groups: control (C), burn (B), diabetes (D), diabetes + burn (DB), diabetes + burn + cream (DBC), and diabetes + burn + ointment (DBP). Each group was further subdivided into 7-day (First subgroups) and 14-day (Second subgroups) treatment subgroups. Diabetes was induced by a single intraperitoneal injection of streptozotocin (55 mg/kg). Second-degree thermal burns (1 cm diameter) were induced on the dorsal skin of rats in the burn groups (B, DB, DBC, and DBP). Following burn induction, the DBC and DBP groups received daily topical treatment with a 2.5% Centella asiatica extract–based cream or ointment, respectively. Necropsies were performed on day 7 in the first subgroups and on day 14 in the second subgroups following burn model induction. Wound healing was evaluated macroscopically and histopathologically, and gene expression levels of TNF-α, FGF-2, EGF, VEGF, and IGF-1 were analyzed using quantitative real-time PCR. Wound areas were significantly larger in the DB group, whereas significant reductions were observed on days 7 and 14 in the treated groups (p < 0.05). Histopathological analysis revealed decreased inflammatory cell infiltration and enhanced fibroblast/fibrocyte density, angiogenesis, and epithelialization in the treated groups. Molecular analyses demonstrated significantly decreased TNF-α and increased FGF-2, EGF, VEGF, and IGF-1 expression in the treated groups compared to the DB group (p < 0.05). In conclusion, treatment with Centella asiatica extract supported healing in a diabetic burn model through anti-inflammatory, regenerative, angiogenic, and epithelializing effects. Notably, molecular analyses demonstrated a previously unreported increase in local IGF-1 levels following Centella asiatica extract treatment, supported by pathological findings.