Abstract
High-mobility group box protein-1 (HMGB-1) plays a central role in the inflammatory network, and uncontrolled chronic inflammation can lead to excessive scarring. The aim of this study was to evaluate the anti-inflammatory effects of polydeoxyribonucleotide (PDRN) on scar formation. Sprague-Dawley rats (n = 30) underwent dorsal excision of the skin, followed by skin repair. PDRN (8 mg/kg) was administered via intraperitoneal injection for three (PDRN-3 group, n = 8) or seven (PDRN-7 group, n = 8) days, and HMGB-1 was administered via intradermal injection in addition to PDRN treatment for three days (PDRN-3+HMGB-1 group; n = 6). The scar-reducing effects of PDRN were evaluated in the internal scar area and by inflammatory cell counts using histology and immunohistochemistry. Western blot, immunohistochemistry and immunofluorescence assays were performed to observe changes in type I and type III collagen and the expression of HMGB-1 and CD45. Treatment with PDRN significantly reduced the scar area, inflammatory cell infiltration and the number of CD45-positive cells. In addition, the increased expression of HMGB-1 observed in the sham group was significantly reduced after treatment with PDRN. Rats administered HMGB-1 in addition to PDRN exhibited scar areas with inflammatory cell infiltration similar to the sham group, and the collagen synthesis effects of PDRN were reversed. In summary, PDRN exerts anti-inflammatory and collagen synthesis effects via HMGB-1 suppression, preventing scar formation. Thus, we believe that the anti-inflammatory and collagen synthesis effects of PDRN resulted in faster wound healing and decreased scar formation.
Highlights
Inflammation is an inevitable first step in the process of wound healing and is closely related to scar formation
We hypothesized that the inhibition of inflammatory cell infiltration could be a factor in reducing scar formation
In the quantitative analysis of the scar area, the scar sizes of the sham, PDRN-3, and PDRN-7 groups were 51,272 ± 5793 μm2, 13,201 ± 2243 μm2, and 21,329 ± 1518 μm2, respectively, on Day 7 of the postoperative period (* p < 0.05, *** p < 0.001; Figure 1C), while, on Day 14 of the postoperative period, the scar sizes decreased to 35,368 ± 3511 μm2, 12,304 ± 1842 μm2, and 13,291 ± 1076 μm2, respectively (** p < 0.01, *** p < 0.001; Figure 1C)
Summary
Inflammation is an inevitable first step in the process of wound healing and is closely related to scar formation. In one prior study involving a scarless fetal wound-healing model, scar formation was caused by the injection of mast cells [5]. Despite the observation that neutrophil depletion did not alter wound-breaking strength or collagen deposition, neutrophil depletion resulted in wounds that healed in a more organized fashion compared with normal wounds [6]. Another previous study revealed that macrophage depletion reduced scar formation [7]. We hypothesized that the inhibition of inflammatory cell infiltration could be a factor in reducing scar formation
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