Usnic acid inhibits hypertrophic scarring in a rabbit ear model by suppressing scar tissue angiogenesis.
Usnic acid inhibits hypertrophic scarring in a rabbit ear model by suppressing scar tissue angiogenesis.
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DOI：
10.1016/j.biopha.2018.06.176
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发表时间：
2018-12
期刊：
影响因子：
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通讯作者：
Yajuan Song;Zhou Yu;Baoqiang Song;Shuzhong Guo;L. Lei;Xianjie Ma;Yingjun Su
中科院分区：
文献类型：
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作者：
Yajuan Song;Zhou Yu;Baoqiang Song;Shuzhong Guo;L. Lei;Xianjie Ma;Yingjun Su
增生性瘢痕是中国人群中的常见疾病;然而，目前没有令人满意的药物来治疗这种疾病。以往的研究表明，血管生成在增生性瘢痕形成的早期阶段起着重要作用，抑制血管生成已被报道为抗增生性瘢痕治疗的有效策略。最近的研究表明，松萝酸（UA），主要存在于地衣中的活性化合物，在体内和体外都能抑制肿瘤血管生成。为探讨尿酸对兔耳增生性瘢痕的治疗作用及其可能机制，建立兔耳增生性瘢痕模型。每周一次用UA、DMSO或醋酸曲安奈德治疗瘢痕，持续四周。苏木精-伊红染色的组织学评价表明，UA显着抑制增生性瘢痕形成，瘢痕高度和着色明显减少。瘢痕隆起指数（SEI）也明显降低。Masson三色染色显示UA可明显改善胶原组织的积聚。免疫组化分析显示，UA能显著抑制瘢痕血管生成。在体外，UA抑制内皮细胞迁移和管形成以及人脐静脉内皮细胞和瘢痕成纤维细胞的增殖。这些结果提供了UA在动物模型中通过涉及抑制瘢痕血管生成的机制在增生性瘢痕形成中的治疗有效性的第一证据。
Hypertrophic scarring is a common condition in the Chinese population; however, there are currently no satisfactory drugs to treat the disorder. Previous studies showed that angiogenesis plays an important role in the early phase of hypertrophic scarring and inhibition of angiogenesis has been reported as an effective strategy for anti-hypertrophic scar therapy. A recent study showed that usnic acid (UA), an active compound found mainly in lichens, inhibited tumor angiogenesis both in vivo and in vitro. To investigate the therapeutic effects of UA on hypertrophic scarring and to explore the possible mechanism involved, a rabbit ear hypertrophic scar model was established. Scars were treated once a week for four weeks with UA, DMSO or triamcinolone acetonide acetate. Histological evaluation of hematoxylin and eosin staining indicated that UA significantly inhibited hypertrophic scar formation, with obvious reductions in scar height and coloration. The scar elevation index (SEI) was also evidently reduced. Masson’s trichrome staining showed that UA significantly ameliorated accumulation of collagen tissue. Immunohistochemical analysis of CD31 expression showed that UA significantly inhibited scar angiogenesis. In vitro, UA inhibited endothelial cell migration and tube formation as well as the proliferation of both human umbilical vein endothelial cells and scar fibroblast cells. These results provide the first evidence of the therapeutic effectiveness of UA in hypertrophic scar formation in an animal model via a mechanism that involves suppression of scar angiogenesis.