生长激素释放肽6促进愈合过程,改善伤口的美观效果。

Plastic Surgery International Pub Date : 2016-01-01 Epub Date: 2016-04-20 DOI:10.1155/2016/4361702
Yssel Mendoza Marí, Maday Fernández Mayola, Ana Aguilera Barreto, Ariana García Ojalvo, Yilian Bermúdez Alvarez, Ana Janet Mir Benítez, Jorge Berlanga Acosta
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引用次数: 4

摘要

除了其细胞保护作用外,生长激素释放肽6 (GHRP-6)被证明可以减轻肝纤维化硬化。CD36作为GHRP-6受体之一,在皮肤创面肉芽组织中大量存在。在CD36激动性刺激的情况下,愈合反应以前没有研究过。Wistar大鼠背部切除全层创面(6 mmØ),每日2次局部治疗,连续5天。建立兔耳增生性瘢痕通用模型,每日治疗30 d。两种植物均采用含有GHRP-6 400 μg/mL的CMC胶浆组合物处理。伤口反应表征包括闭合动态,RT-PCR转录谱,组织学和组织形态测量程序。大鼠实验表明,GHRP-6的药效学涉及免疫炎症介质及其效应细胞的衰减,以及纤维化细胞因子表达的减少。重要的是,在肥厚性疤痕兔模型中,GHRP-6干预通过激活PPARγ和降低纤维原性细胞因子的表达,显著减少了增生疤痕的发生。GHRP-6对巩固性病变的逆转无影响。这一证据支持了CD36是一种活性的、药理学上可接近的受体,可以减轻伤口炎症并加速其关闭,从而改善伤口美观。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Growth Hormone-Releasing Peptide 6 Enhances the Healing Process and Improves the Esthetic Outcome of the Wounds.

Growth Hormone-Releasing Peptide 6 Enhances the Healing Process and Improves the Esthetic Outcome of the Wounds.

Growth Hormone-Releasing Peptide 6 Enhances the Healing Process and Improves the Esthetic Outcome of the Wounds.

Growth Hormone-Releasing Peptide 6 Enhances the Healing Process and Improves the Esthetic Outcome of the Wounds.

In addition to its cytoprotective effects, growth hormone-releasing peptide 6 (GHRP-6) proved to reduce liver fibrotic induration. CD36 as one of the GHRP-6 receptors appears abundantly represented in cutaneous wounds granulation tissue. The healing response in a scenario of CD36 agonistic stimulation had not been previously investigated. Excisional full-thickness wounds (6 mmØ) were created in the dorsum of Wistar rats and topically treated twice a day for 5 days. The universal model of rabbit's ears hypertrophic scars was implemented and the animals were treated daily for 30 days. Treatments for both species were based on a CMC jelly composition containing GHRP-6 400 μg/mL. Wounds response characterization included closure dynamic, RT-PCR transcriptional profile, histology, and histomorphometric procedures. The rats experiment indicated that GHRP-6 pharmacodynamics involves attenuation of immunoinflammatory mediators, their effector cells, and the reduction of the expression of fibrotic cytokines. Importantly, in the hypertrophic scars rabbit's model, GHRP-6 intervention dramatically reduced the onset of exuberant scars by activating PPARγ and reducing the expression of fibrogenic cytokines. GHRP-6 showed no effect on the reversion of consolidated lesions. This evidence supports the notion that CD36 is an active and pharmacologically approachable receptor to attenuate wound inflammation and accelerate its closure so as to improve wound esthetic.

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