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口服积雪草苷抑制兔耳瘢痕模型的瘢痕增生。

Inhibition of hypertrophic scar formation with oral asiaticoside treatment in a rabbit ear scar model.

机构信息

Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Shanghai Key Laboratory of Tissue Engineering Research, Shanghai, China.

出版信息

Int Wound J. 2021 Oct;18(5):598-607. doi: 10.1111/iwj.13561. Epub 2021 Mar 5.

DOI:10.1111/iwj.13561
PMID:33666348
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8450800/
Abstract

Hypertrophic scar (HS) is a fibrotic skin disease characterised by over-productive collagen and excessive inflammatory reaction, which can be functionally and cosmetically problematic. A scar-prone constitute will accelerate HS formation and functional disorder, which deserves systemic therapy with oral medicine. To examine the oral therapeutic effectiveness on HS with convincing evidence of gross view and histological improvement, a rabbit ear HS model was employed with oral administration of asiaticoside (AS) at the doses of 12 and 24 mg kg  d daily for 60 consecutive days. Gross observation and histological findings showed that oral AS treatment could significantly inhibit HS formation in a dose dependent manner. Semi-quantification of scar elevation index at days 7, 15, 30, and 60, and quantitative polymerase chain reaction at days 30 and 60 also provided the evidences of reduced scar thickness and inhibited fibrotic gene expressions of collagens I, III, TGF-β1, interleukins 1β, 6 and 8, and enhanced gene expression of SMAD 7 and PPAR-γ with a dose-dependent manner. These results indicated that AS is likely to serve as a systemic therapeutic agent of HS treatment for those who may have scar-prone constitute via anti-inflammation, inhibiting fibrotic process, and enhancing matrix degradation.

摘要

增生性瘢痕(HS)是一种以胶原过度产生和过度炎症反应为特征的纤维化皮肤疾病,可能会导致功能和美容问题。易形成瘢痕的体质会加速 HS 的形成和功能障碍,需要全身性治疗,包括口服药物。为了用宏观和组织学改善的令人信服的证据来检验 HS 的口服治疗效果,采用兔耳 HS 模型,每天口服积雪草苷(AS)12 和 24mg/kg,连续 60 天。宏观观察和组织学发现,AS 治疗可显著抑制 HS 的形成,呈剂量依赖性。第 7、15、30 和 60 天的瘢痕隆起指数半定量分析以及第 30 和 60 天的定量聚合酶链反应也提供了证据,表明 AS 可减少瘢痕厚度,抑制胶原 I、III、TGF-β1、白细胞介素 1β、6 和 8 的纤维化基因表达,并增强 SMAD7 和 PPAR-γ的基因表达,呈剂量依赖性。这些结果表明,AS 可能通过抗炎、抑制纤维化过程和增强基质降解,作为治疗易形成瘢痕体质的 HS 的全身性治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/8450800/679835b90a75/IWJ-18-598-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/8450800/57931fc88637/IWJ-18-598-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/8450800/c612052e074c/IWJ-18-598-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/8450800/f868ff4eb21a/IWJ-18-598-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/8450800/679835b90a75/IWJ-18-598-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/8450800/57931fc88637/IWJ-18-598-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/8450800/c612052e074c/IWJ-18-598-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/8450800/f868ff4eb21a/IWJ-18-598-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a943/8450800/679835b90a75/IWJ-18-598-g003.jpg

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