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首页> 外文期刊>Archives of dermatological research. >Protection against TGF-β1-induced fibrosis effects of IL-10 on dermal fibroblasts and its potential therapeutics for the reduction of skin scarring.
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Protection against TGF-β1-induced fibrosis effects of IL-10 on dermal fibroblasts and its potential therapeutics for the reduction of skin scarring.

机译：防止TGF-β1诱导的IL-10对皮肤成纤维细胞的纤维化作用及其潜在的减少皮肤瘢痕形成的疗法。

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摘要

Scarring, tightly associated with fibrosis, is a significant symptomatic clinical problem. Interleukin 10 (IL-10) has been identified as a candidate scar-improving therapy based on preclinical studies. However, the molecular mechanism of IL-10 in scar improvement is still uncertain. In this study, human dermal fibroblasts stimulated with TGF-β1 were treated with IL-10 to analyze the mRNA and some of proteins' expression levels of type I collagen (Col1), type III collagen (Col3), alpha-smooth muscle actin (α-SMA), matrix metalloproteinase-1 (MMP1), MMP2, MMP8 and tissue inhibitor of metalloproteinase 1 (TIMP1), TIMP2 by real-time PCR and Western blot, to observe α-SMA-positive fibroblasts by immunocytochemistry. The contracture and improvement of fibroblast-populated collagen lattice (FPCL) and a murine model of wound healing were used to evaluate the scar-improving effects by histological staining. The results showed that IL-10 can significantly down-regulate the mRNA and protein expression levels of Col1, Col3, α-SMA, and up-regulate the mRNA expression levels of MMP1 and MMP8, and decrease α-SMA-positive fibroblasts. FPCL analysis showed that the IL-10 (20?ng/ml) can significantly inhibit the contracture, improve the architecture of FPCL. Wounds injected with IL-10 demonstrated that the appearance of scar was improved, the wound margin of scarring was narrow, and the deposition of collagens (Col1 and Col3) in regenerated tissue was relieved. These results provide direct evidences that IL-10 has the inhibitory effects on the excessive deposition of extracellular matrix components and fibroblast-to-myofibroblast transition, and show that IL-10 has the potential therapy in prevention and reduction of skin scarring.
机译：与纤维化紧密相关的瘢痕形成是一个重要的症状性临床问题。根据临床前研究，白介素10（IL-10）已被确认为候选疤痕改善疗法。但是，IL-10改善瘢痕的分子机制仍不确定。在这项研究中，用TGF-β1刺激的人类皮肤成纤维细胞用IL-10处理，以分析I型胶原蛋白（Col1），III型胶原蛋白（Col3），α平滑肌肌动蛋白（ α-SMA），基质金属蛋白酶1（MMP1），MMP2，MMP8和金属蛋白酶1组织抑制剂（TIMP1），TIMP2通过实时PCR和Western blot观察，通过免疫细胞化学观察α-SMA阳性成纤维细胞。使用成纤维细胞填充的胶原蛋白晶格（FPCL）的挛缩和改善以及小鼠伤口愈合模型，通过组织学染色评估疤痕改善效果。结果表明，IL-10可以显着下调Col1，Col3，α-SMA的mRNA和蛋白表达水平，并上调MMP1和MMP8的mRNA表达水平，并降低α-SMA阳性成纤维细胞。 FPCL分析表明，IL-10（20？ng / ml）可以显着抑制挛缩，改善FPCL的结构。注射IL-10的伤口表明，瘢痕的外观得到改善，瘢痕的伤口边缘狭窄，并且再生组织中胶原蛋白（Col1和Col3）的沉积得到缓解。这些结果提供了直接的证据，证明IL-10对细胞外基质成分的过度沉积和成纤维细胞向成肌纤维细胞的转化具有抑制作用，并表明IL-10在预防和减少皮肤瘢痕形成方面具有潜在的治疗作用。

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