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乌苏酸通过抑制瘢痕组织血管生成抑制兔耳增生性瘢痕。

Usnic acid inhibits hypertrophic scarring in a rabbit ear model by suppressing scar tissue angiogenesis.

机构信息

Department of Plastic and Reconstructive Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.

Department of Plastic and Reconstructive Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.

出版信息

Biomed Pharmacother. 2018 Dec;108:524-530. doi: 10.1016/j.biopha.2018.06.176. Epub 2018 Sep 20.

DOI:10.1016/j.biopha.2018.06.176
PMID:30243085
Abstract

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.

摘要

增生性瘢痕在中国人群中很常见;然而,目前还没有满意的药物来治疗这种疾病。先前的研究表明,血管生成在增生性瘢痕的早期阶段起着重要作用,抑制血管生成已被报道为一种有效的抗增生性瘢痕治疗策略。最近的一项研究表明,松萝酸(UA),一种主要存在于地衣中的活性化合物,在体内和体外均能抑制肿瘤血管生成。为了研究 UA 对增生性瘢痕的治疗效果,并探讨其可能的作用机制,建立了兔耳增生性瘢痕模型。UA、DMSO 或曲安奈德醋酸酯每周治疗一次,共 4 周。苏木精-伊红染色的组织学评价表明,UA 显著抑制增生性瘢痕的形成,明显降低了瘢痕的高度和颜色。瘢痕隆起指数(SEI)也明显降低。Masson 三色染色显示,UA 显著改善了胶原组织的堆积。CD31 表达的免疫组化分析表明,UA 显著抑制了瘢痕血管生成。在体外,UA 抑制了内皮细胞的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。这些结果首次提供了 UA 通过抑制瘢痕血管生成的机制在动物模型中对增生性瘢痕形成具有治疗效果的证据。

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