Rosuvastatin accelerates the healing process of partial-thickness burn wounds in rats by reducing TNF-α levels.

Introduction: Burn wound healing is a complex, dynamic process that involves a coordinated cascade of cellular responses and phases. Inflammation, proliferation and remodeling are the main phases of tissue repair, while tumor necrosis factor α (TNF-α) and procalcitonin (PCT) seem to be important mediators affecting the inflammatory state. Our aim was to assess the effect of rosuvastatin on tissue repair after partial thickness burn injury in healthy animals. Material and methods: In this randomized prospective experimental study, 36 male rats were randomly divided into two groups: placebo-treated (PG) and topical rosuvastatin-treated (SG). Under anesthesia, a partial-thickness burn trauma was induced in the dorsal region of the rats using an iron seal. Tissue samples were collected for histopathological examination as well. Results: Variables of TNF-α, procalcitonin and macroscopic assessment were normally distributed between the two groups on all studied days. The expression of TNF-α was found to be lower in burn injuries treated with topical rosuvastatin in comparison with placebo-treated animals on days 3, 6 and 9. PCT values in rosuvastatin-treated subgroups were statistically significantly lower than in placebo subgroups. Upon macroscopic examination, a significantly smaller burnt area in the statin-treated group was detected compared to the non-statin group on all days, except for day 3. Histopathological examination demonstrated higher levels of mean neutrophil infiltration in the placebo group (day 3). Finally, fibroblast proliferation, angiogenesis and re-epithelization levels were noted to be higher after the topical application of rosuvastatin. Conclusions: Rosuvastatin accelerated wound healing and down-regulated TNF-α and PCT levels.