Xu Lianji, Choi Tae Hyun, Kim Sukwha, Kim Sang-Hyon, Chang Hyuk Won, Choe Misun, Kwon Sun Young, Hur Ji An, Shin Sung Chul, Chung Jong Il, Kang Dawon, Zhang Duo
From the *Department of Plastic and Reconstructive Surgery, Seoul National University College of Medicine, Seoul, Republic of Korea; Departments of †Internal Medicine, ‡Diagnostic Radiology, and §Pathology, Keimyung University Dongsan Medical Center, Daegu, Republic of Korea; ∥Department of Internal Medicine, School of Medicine, Yeungnam University, Daegu, Republic of Korea; Departments of ¶Chemisty, and #Agronomy, Research Institute of Life Science, Gyeongsang National University, Jinju, Republic of Korea; **Department of Physiology, Institute of Health Sciences, College of Medicine, Gyeongsang National University, Jinju, Republic of Korea; and ††Department of Plastic and Reconstructive Surgery, Jilin University, Changchun, China.
Ann Plast Surg. 2013 Oct;71(4):415-20. doi: 10.1097/SAP.0b013e31824ca62b.
Anthocyanins are known to have antioxidant and antiinflammatory effects. We hypothesized that anthocyanins would enhance wound healing in Sprague-Dawley rats. The purpose of this study was to evaluate our hypothesis and investigate the mechanism of wound healing enhancement. The cytoprotective effect of an immortalized epidermal keratinocyte cell line (HaCaT) and human neonatal dermal fibroblasts in response to various concentrations of anthocyanins was determined. Vascular endothelial growth factor (VEGF) and thrombospondin 1 (TSP1) of HaCaT were measured by Western blot analysis. Anthocyanins were applied to the wounds in rats, and the healing ratio was calculated. Tissue VEGF, TSP1, CD31, nuclear factor-κB, and phosphorylation of IκBα were measured. The viability of the HaCaT cell line and human neonatal dermal fibroblasts increased under cytotoxicity by H2O2 in the anthocyanin-treated groups. The VEGF in the anthocyanin-treated groups increased, whereas TSP1 decreased. Wounds in the experimental groups healed faster, and VEGF and CD31 increased in the experimental groups, whereas TSP1 decreased. Anthocyanins inhibited the translocation of nuclear factor-κB (p65) from cytosol to nucleus and also prevented the phosphorylation of IκBα. Anthocyanins enhance wound healing through a cytoprotective effect, enhancement of angiogenesis, and an antiinflammatory effect.
已知花青素具有抗氧化和抗炎作用。我们假设花青素会促进斯普拉格-道利大鼠的伤口愈合。本研究的目的是评估我们的假设并探究伤口愈合增强的机制。测定了永生化表皮角质形成细胞系（HaCaT）和人新生儿真皮成纤维细胞对不同浓度花青素的细胞保护作用。通过蛋白质免疫印迹分析测定HaCaT细胞的血管内皮生长因子（VEGF）和血小板反应蛋白1（TSP1）。将花青素应用于大鼠伤口，并计算愈合率。测定组织中的VEGF、TSP1、CD31、核因子-κB以及IκBα的磷酸化水平。在花青素处理组中，HaCaT细胞系和人新生儿真皮成纤维细胞在H2O2诱导的细胞毒性下活力增加。花青素处理组中的VEGF增加，而TSP1减少。实验组的伤口愈合更快，实验组中的VEGF和CD31增加，而TSP1减少。花青素抑制核因子-κB（p65）从细胞质向细胞核的转位，并阻止IκBα的磷酸化。花青素通过细胞保护作用、促进血管生成和抗炎作用来增强伤口愈合。
