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We examined the effects of photobiomodulation (PBM) independently and combined with curcumin on stereological parameters and basic fibroblast growth factor (bFGF), hypoxia‐inducible factor‐1α (HIF‐1α), and stromal cell‐derived factor‐1α (SDF‐1α) gene expressions in an excisional wound model of rats with type one diabetes mellitus (T1DM). T1DM was induced by an injection of streptozotocin (STZ) in each of the 90 male Wistar rats. One round excision was generated in the skin on the back of each of the 108 rats. The rats were divided into six groups (n = 18 per group): control (diabetic), untreated group; vehicle (diabetic) group, which received sesame oil; PBM (diabetic) group; curcumin (diabetic) group; PBM + curcumin (diabetic) group; and a healthy control group. On days 4, 7, and 15, we conducted both stereological and quantitative real‐time PCR (qRT‐PCR) analyses. The PBM and PBM + curcumin groups had significantly better inflammatory response modulation in terms of macrophages (P < .01), neutrophils (P < .001), and increased fibroblast values compared with the other groups at day 4 (P < .001), day 7 (P < .01), and day 15 (P < .001). PBM treatment resulted in increased bFGF gene expression on days 4 (P < .001) and 7 (P < .001), and SDF‐1α gene expression on day 4 (P < .001). The curcumin group had increased bFGF (P < .001) expression on day 4. Both the PBM and PBM + curcumin groups significantly increased wound healing by modulation of the inflammatory response, and increased fibroblast values and angiogenesis. The PBM group increased bFGF and SDF‐1α according to stereological and gene expression analyses compared with the other groups. The PBM and PBM + curcumin groups significantly increased the skin injury repair process to more rapidly reach the proliferation phase of the wound healing in T1DM rats.

Introduction: Abnormal wound repair is a cause for considerable expense, as well as patient morbidity and mortality. Here, we investigated the combined impact of photobiomodulation (PBM) and curcumin on a rat experimental model of an acute skin wound. Methods: A round full-thickness wound was created on the back of each rat. We divided the rats into the following four groups. Group one was the control group. Group two received pulse wave (PW) PBM at a dose of 890 nm, 80 Hz, and 0.2 J/cm2 . Group 3 received 40 mg/kg curcumin by gastric gavage and group 4 were treated with PWPBM + curcumin. We measured the wound area on days 4, 7, and 15, and performed microbiological and tensiometric examinations. Results: There was markedly improved wound contraction in the curcumin (7.5 ± 0.57; P=0.000), PBM (8.5 ± 1.2; P=0.000), and PBM + curcumin (14.5 ± 4.3; P=0.002) groups relative to the control group (25 ± 6). PBM (100 ± 7.3; P=0.005), and PBM + curcumin (98 ± 6; P=0.005) groups meaningfully improved tensile strength relative to the control group (61 ± 8.2). On day 15, the PBM (10 ± 5; P=0.000), curcumin (14 ± 4.5, P=0.000), and PBM + curcumin (27.3 ± 8.3; P=0.000) groups meaningfully decreased microbial flora relative to the control group (95 ± 6). Conclusion: We concluded that the PBM and PBM + curcumin groups meaningfully accelerated wound healing of the acute skin wound in the rats. The results of the PBM group were statistically more effective than the curcumin alone and PBM + curcumin-treated groups.

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