首页> 外文期刊>Journal of periodontal research >Nitric oxide synthase type-II is synthesized by human gingival tissue and cultured human gingival fibroblasts.
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Nitric oxide synthase type-II is synthesized by human gingival tissue and cultured human gingival fibroblasts.

机译:通过人牙龈组织和培养的人牙龈成纤维细胞合成一氧化氮合酶型II。

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摘要

Nitric oxide is known to be an important inflammatory mediator, and is implicated in the pathophysiology of a range of inflammatory disorders. The aim of this study was to determine the localization and distribution of endothelial NOS (NOS-II) in human gingival tissue, and to ascertain if human gingival fibroblasts express NOS-II when stimulated with interferon gamma (IFN-gamma) and bacterial lipopolysaccharide (LPS). The distribution of NOS-II in inflamed and non-inflamed specimens of human gingivae was studied using a monoclonal antibody against nitric oxide synthase II. Cultures of fibroblasts derived from healthy human gingivae were used for the cell culture experiments. The results from immunohistochemical staining of the tissues indicated an upregulation of NOS-II expression in inflamed compared to non-inflamed gingival tissue. Fibroblasts and inflammatory cells within the inflamed connective tissue were positively stained for NOS-II. In addition, basal keratinocytes also stained strongly for NOS-II, in both healthy and inflamed tissue sections. When cultured human gingival fibroblasts were stimulated by INF-gamma and Porphyromonas gingivalis LPS, NOS-II was more strongly expressed than when the cells were exposed to LPS or IFN-gamma alone. These data suggest that, as for other inflammatory diseases, NO plays a role in the pathophysiology of periodontitis.
机译:已知一氧化氮是重要的炎症介质,并且涉及一系列炎性病症的病理生理学。本研究的目的是确定人牙龈组织中内皮NOS(NOS-II)的定位和分布,并确定当用干扰素γ(IFN-GAMMA)和细菌脂多糖刺激时人牙龈成纤维细胞表达NOS-II( lps)。使用对一氧化氮合酶II的单克隆抗体研究了人牙龈发炎和非发炎标本的NOS-II的分布。衍生自健康人牙苷的成纤维细胞的培养用于细胞培养实验。由组织的免疫组织化学染色的结果表明,与非发炎的牙龈组织相比,发炎的NOS-II表达的上调性。发炎结缔组织内的成纤维细胞和炎症细胞用于NOS-II呈正染色。此外,基础角蛋白细胞也强烈染色,在健康和发炎的组织切片中。当培养的人牙龈成纤维细胞被INF-γ和卟啉核糖菌刺激时,NOS-II更强烈地表达,而不是单独将细胞暴露于LPS或IFN-Gamma时。这些数据表明,如其他炎症性疾病,在牙周炎的病理生理学中没有发挥作用。

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