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首页> 外文期刊>Journal of dermatological science >Differential down-regulation of COX-2 and MMP-13 in human skin fibroblasts by glucosamine-hydrochloride.
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Differential down-regulation of COX-2 and MMP-13 in human skin fibroblasts by glucosamine-hydrochloride.

机译：盐酸氨基葡萄糖对人皮肤成纤维细胞中COX-2和MMP-13的差异性下调。

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BACKGROUND: Evidence suggests anti-inflammatory effects of glucosamine (GS) on inflammatory diseases. COX-2 is an enzyme to produce prostaglandins. MMPs are the family of matrix metalloproteinases degradable of ECM. Excess expression of COX-2 or MMPs involves in skin inflammation. OBJECTIVE: We evaluated whether GS-HCl modulates expression of COX-2 and/or MMPs by IL-1beta or PMA in human skin fibroblasts (HSF) or keratinocytes (HaCaT). METHODS: HSF or HaCaT cells were exposed to IL-1beta or PMA without or with GS-HCl. COX-2 or MMPs protein and mRNA expression, respectively, were analyzed by Western blot and RT-PCR. MTS assay was utilized to assess the cytotoxicity of GS-HCl on HSF cells. RESULTS: In HSF cells, IL-1beta treatment induced COX-2 and MMP-13 expressions in association with activation of ERKs, p38 MAPK, JNKs, and NF-kappaB. PMA treatment also induced COX-2 and MMP-13 expressions in association with p38 MAPK activation. Of interest, treatment with GS-HCl (10mM) led to blockage of p38 MAPK activation, accumulation of 66kDa COX-2 protein variant (without affecting COX-2 mRNA expression), and transcriptional down-regulation of MMP-13 in the IL-1beta- or PMA-treated HSF cells. Distinctly, pharmacological inhibition of p38 MAPK with SB203580 was associated with transcriptional down-regulation of COX-2 and MMP-13 in the IL-1beta- or PMA-treated HSF cells. In addition, the GS-HCl-mediated COX-2 protein modification was observed in both endogenous and PMA-induced COX-2 in HaCaT cells. CONCLUSIONS: GS-HCl differentially down-regulates COX-2 and MMP-13 expression in the IL-1beta- or PMA-treated human skin fibroblasts via the p38 MAPK-independent COX-2 translational inhibition and the p38 MAPK-dependent MMP-13 transcriptional suppression, respectively.
机译：背景：有证据表明，葡萄糖胺（GS）对炎性疾病具有抗炎作用。 COX-2是产生前列腺素的酶。 MMP是ECM可降解的基质金属蛋白酶家族。 COX-2或MMPs的过量表达涉及皮肤炎症。目的：我们评估了GS-HCl是否能调节人皮肤成纤维细胞（HSF）或角质形成细胞（HaCaT）中IL-1beta或PMA对IL-1beta或PMA的COX-2和/或MMPs表达的影响。方法：HSF或HaCaT细胞暴露于IL-1beta或PMA，无或含GS-HCl。通过蛋白质印迹和RT-PCR分别分析COX-2或MMPs的蛋白质和mRNA表达。 MTS测定法用于评估GS-HCl对HSF细胞的细胞毒性。结果：在HSF细胞中，IL-1β处理可诱导ERK，p38 MAPK，JNK和NF-κB活化，从而诱导COX-2和MMP-13表达。 PMA治疗还诱导了COX-2和MMP-13的表达与p38 MAPK激活相关。有趣的是，用GS-HCl（10mM）处理可导致p38 MAPK活化受阻，66kDa COX-2蛋白变体积聚（不影响COX-2 mRNA表达）以及IL-中MMP-13的转录下调。 1beta或PMA处理的HSF细胞。明显地，用SB203580抑制p38 MAPK的药理作用与IL-1β或PMA处理的HSF细胞中COX-2和MMP-13的转录下调有关。此外，在HaCaT细胞的内源性和PMA诱导的COX-2中均观察到了GS-HCl介导的COX-2蛋白修饰。结论：GS-HCl通过不依赖p38 MAPK的COX-2翻译抑制和依赖p38 MAPK的MMP-13差异下调IL-1beta或PMA处理的人皮肤成纤维细胞中COX-2和MMP-13的表达。转录抑制。

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