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首页> 外文期刊>Mediators of inflammation >Carbon Monoxide-Releasing Molecule-3 Suppresses Tumor Necrosis Factor-α- and Interleukin-1β-Induced Expression of Junctional Molecules on Human Gingival Fibroblasts via the Heme Oxygenase-1 Pathway
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Carbon Monoxide-Releasing Molecule-3 Suppresses Tumor Necrosis Factor-α- and Interleukin-1β-Induced Expression of Junctional Molecules on Human Gingival Fibroblasts via the Heme Oxygenase-1 Pathway

机译：一氧化碳释放分子-3抑制肿瘤坏死因子-α-和白细胞介素-1β诱导的在人牙龈成纤维细胞上通过血红素氧合酶-1途径诱导了结分子的表达

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Human gingival fibroblast barrier dysfunction caused by inflammation contributes to gingivitis and can lead to inflammatory periodontal disease. The disease features include upregulated epithelial permeability, increased inflammatory mediators, and downregulated junctional complex molecules. Carbon monoxide- (CO-) releasing molecule-3 (CORM-3) is a water-soluble compound that has demonstrated anti-inflammatory effects in in vitro and in vivo studies. In this study, we aimed to investigate the effects of CORM-3 on the expression of tight and adherens junction molecules on human gingival fibroblasts (HGFs) stimulated with tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). HGFs were cultured from the explants of normal human gingival tissues, which were stimulated in the presence or absence of CORM-3. Epithelial barrier function was evaluated by paracellular permeability and junctional complex molecule expression analyses. The protein and mRNA expression levels of adherens junction molecules (VE-cadherin and β-catenin) and tight junction molecules (zona occludens-1, ZO-1) were studied using western blot analysis and reverse transcription-quantitative polymerase chain reaction (RT-PCR). The mRNA and protein expression levels of these cytokines were also analyzed in HGFs transiently transfected with HO-1 small interfering RNA (siRNA) in response to TNF-α and IL-1β stimulation. CORM-3 reduced permeability and enhanced the expression of junctional complex molecules (ZO-1, VE-cadherin, and β-catenin) in TNF-α- and IL-1β-induced HGFs. However, these effects of CORM-3 were attenuated when HO-1 siRNA was transiently transfected in HGFs. These findings indicate that CORM-3 exerts anti-inflammatory effects on TNF-α- and IL-1β-stimulated HGFs via the HO-1 pathway, which suggests the promising potential of CORM-3 in the treatment of inflammatory periodontal disease.
机译：炎症引起的人牙龈成纤维细胞功能障碍有助于牙龈炎，可导致炎症牙周病。该疾病特征包括上翘渗透性，增加的炎症介质和下调的连接复合分子。释放分子-3（COM-3）的一氧化碳 - （共）释放分子-3是一种水溶性化合物，其在体外和体内研究中表现出抗炎作用。在这项研究中，我们旨在探讨CINM-3对用肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）刺激的人牙龈成纤维细胞（HGFS）表达的粘附和粘附结分子的影响）。从正常人体牙龈组织的外植体培养HGF，这些植物在存在或不存在CINM-3时受到刺激。通过细胞间渗透性和结络合物表达分析评估上皮屏障功能。使用蛋白质印迹分析和逆转录定量聚合酶链反应研究粘附结分子（Ve-Cadherin和β-Catenin）和紧密结分子（Zona Occludens-1，ZO-1）的蛋白质和mRNA表达水平（Zona occludens-1，ZO-1）（Rt- PCR）。在响应于TNF-α和IL-1β刺激的HGFS瞬时转染的HGF中，还分析了这些细胞因子的mRNA和蛋白表达水平。肠胃3降低渗透性并增强了TNF-α-和IL-1β诱导的HGF中的结络合物分子（ZO-1，Ve-Cadherin和β-Catenin）的表达。然而，当HO-1 siRNA在HGF中瞬时转染时，肝-3的这些效果衰减。这些发现表明，CINT-3通过HO-1途径对TNF-α-和IL-1β刺激的HGF产生抗炎作用，这表明CORM-3在治疗炎症牙周病方面的有希望的潜力。

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