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首页> 外文期刊>Pharmacological research: The official journal of The Italian Pharmacological Society >The effect of hyaluronic acid on interleukin-1-induced deregulation of collagen metabolism in cultured human skin fibroblasts.
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The effect of hyaluronic acid on interleukin-1-induced deregulation of collagen metabolism in cultured human skin fibroblasts.

机译：透明质酸对培养的人皮肤成纤维细胞中白介素1诱导的胶原代谢失调的影响。

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摘要

Although hyaluronic acid (HA) has been used in the treatment of osteoarthritis for 30 years, the mechanism of its protective action on collagen metabolism disturbances in tissues during inflammation is not known. The present study was undertaken to evaluate the mechanism of Interleukin-1 (IL-1)-induced deregulation of collagen metabolism in cultured human skin fibroblast and the effect of HA on the process. In normal fibroblasts IL-1 strongly induced inhibition of collagen biosynthesis, while HA counteracted the process. The mechanism of this phenomenon was independent of prolidase activity, an enzyme that plays an important role in collagen biosynthesis at the post-translational level. Instead, IL-1 was found to inhibit the expression of insulin-like growth factor-I receptor (IGF-IR) and MAP kinases-ERK1 and ERK2, while HA was shown to counteract this process. Since insulin-like growth factor-I (IGF-I) is a most potent stimulator of collagen biosynthesis in fibroblasts the mechanism of IL-1-dependent inhibition of collagen biosynthesis may be related to inhibition of IGF-IR expression and signaling. The data suggest that hyaluronic acid protects collagen against IL-1-induced inhibition of biosynthesis of this protein in cultured human skin fibroblasts at the level of IGF-IR signaling.
机译：尽管透明质酸（HA）在骨关节炎的治疗中已经使用了30年，但其对炎症过程中组织胶原代谢紊乱的保护作用机理尚不清楚。本研究旨在评估白介素-1（IL-1）诱导的培养人皮肤成纤维细胞胶原代谢失调的机制以及HA对这一过程的影响。在正常的成纤维细胞中，IL-1强烈诱导了胶原生物合成的抑制作用，而HA则抵消了这一过程。这种现象的机制与蛋白水解酶活性无关，该酶在翻译后水平上在胶原生物合成中起重要作用。相反，发现IL-1抑制胰岛素样生长因子-I受体（IGF-IR）和MAP激酶-ERK1和ERK2的表达，而HA被证明可以抵消这一过程。由于胰岛素样生长因子-I（IGF-1）是成纤维细胞中胶原蛋白生物合成的最有效刺激剂，因此依赖IL-1的胶原蛋白生物合成抑制机制可能与抑制IGF-1R表达和信号传导有关。数据表明，透明质酸在IGF-IR信号传导水平上保护胶原蛋白免受IL-1诱导的该蛋白在培养的人皮肤成纤维细胞中的生物合成抑制。

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