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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治疗，用于减少皮肤瘢痕。

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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：疤痕，与纤维化紧密相关，是一个重要的症状临床问题。白细胞介素10（IL-10）已被鉴定为基于临床前研究的候选瘢痕改善治疗。然而，IL-10在瘢痕改善中的分子机制仍然不确定。在该研究中，用IL-10处理用TGF-β1刺激的人的皮肤成纤维细胞以分析MRNA和一些蛋白质表达水平的I型胶原（COL1），III型胶原（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（TIMP1），TIMP2通过实时PCR和Western印迹，观察免疫细胞化学观察α-SMA阳性成纤维细胞。使用成纤维细胞植物胶原晶格（FPCL）的挛缩和改善伤口愈合的鼠模型来评估组织学染色的瘢痕改善。结果表明，IL-10可以显着降低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（20μg/ ml）可以显着抑制挛缩，改善FPCL的结构。注射IL-10的伤口证明了瘢痕的出现改善，瘢痕突的伤口裕度窄，并且抑制了再生组织中的胶原（COL1和COL3）的沉积。这些结果提供了直接证据，即IL-10对细胞外基质组分和成纤维细胞对肌纤维细胞转变的过度沉积具有抑制作用，并且表明IL-10具有预防和减少皮肤瘢痕的潜在疗法。

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