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组蛋白去乙酰化酶抑制剂可减少兔耳模型中的增生性瘢痕形成。

Histone deacetylase inhibitor reduces hypertrophic scarring in a rabbit ear model.

机构信息

Xi'an and Luzhou, People's Republic of China From the Departments of Plastic Surgery and Pathology, Xijing Hospital, Fourth Military Medical University; and the Department of Blood Transfusion, Affiliated Hospital of Luzhou Medical College.

出版信息

Plast Reconstr Surg. 2013 Jul;132(1):61e-69e. doi: 10.1097/PRS.0b013e318290f698.

DOI:10.1097/PRS.0b013e318290f698
PMID:23806955
Abstract

BACKGROUND

Hypertrophic scars result from excessive collagen deposition at sites of healing dermal wounds and could be functionally and cosmetically problematic. The authors tested the ability of the histone deacetylase inhibitor trichostatin A to reduce hypertrophic scar formation in a rabbit ear model.

METHODS

The authors have developed a reliable rabbit model that results in hypertrophic scarring. Four 1-cm, full-thickness, circular wounds were made on each ear. After the wounds reepithelialized, 0.02% trichostatin A was injected intradermally into the wounds in the treatment group. Expression of collagen I and fibronectin was detected by reverse transcription polymerase chain reaction and Western blot analysis at postoperative day 23. Scar hypertrophy was quantified by measurement of the scar elevation index at postoperative day 45.

RESULTS

Compared with the control group, injection of trichostatin A led to much more normal-appearing scars in the rabbit ear. The scar elevation index at postoperative day 45 was significantly decreased after injection of trichostatin A compared with untreated scars. Furthermore, the authors confirmed the decreased expression of collagen I and fibronectin at postoperative day 23 (after the rabbits had been treated with trichostatin A for 1 week) in the treated scars compared with the control scars according to reverse transcription polymerase chain reaction and Western blot analysis.

CONCLUSIONS

The introduction of trichostatin A can result in the decreased formation of hypertrophic scars in a rabbit ear model, which is corroborated by evidence of decreased collagen I and fibronectin synthesis.

摘要

背景

增生性瘢痕是由于真皮伤口愈合部位胶原过度沉积而引起的,可能会导致功能和美容问题。作者测试了组蛋白去乙酰化酶抑制剂曲古抑菌素 A 减少兔耳模型中增生性瘢痕形成的能力。

方法

作者开发了一种可靠的兔模型,该模型会导致增生性瘢痕形成。每个耳朵上制作 4 个 1cm 全层、圆形的伤口。当伤口再上皮化后,将 0.02%的曲古抑菌素 A 皮内注射到治疗组的伤口中。术后第 23 天通过逆转录聚合酶链反应和 Western blot 分析检测胶原 I 和纤维连接蛋白的表达。术后第 45 天通过测量瘢痕隆起指数来量化瘢痕增生。

结果

与对照组相比,曲古抑菌素 A 的注射使兔耳的瘢痕外观更正常。与未经处理的瘢痕相比,曲古抑菌素 A 注射后术后第 45 天的瘢痕隆起指数显著降低。此外,根据逆转录聚合酶链反应和 Western blot 分析,作者证实了在接受曲古抑菌素 A 治疗 1 周后的治疗瘢痕中,胶原 I 和纤维连接蛋白的表达降低。

结论

在兔耳模型中引入曲古抑菌素 A 可导致增生性瘢痕形成减少,这一结论得到了胶原 I 和纤维连接蛋白合成减少的证据的支持。

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