中山醫學大學機構典藏 CSMUIR:Item 310902500/11342
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    题名: The up-regulation of heme oxygenase-1 expression in human gingival fibroblasts stimulated with nicotine.
    作者: Chang, YC
    Lai, CC
    Lin, LF
    Ni, WF
    Tsai, CH
    贡献者: 中山醫學大學
    日期: 2005
    上传时间: 2015-07-15T10:48:39Z (UTC)
    ISSN: 0022-3484
    摘要: BACKGROUND:
    Cigarette smoking is a major risk factor in the development and further progression of periodontal diseases. Heme oxygenase-1 (HO-1) is known as a stress-inducible protein and functions as an antioxidant enzyme. There is limited information on the expression of HO-1 in smoking-associated periodontal disease.
    OBJECTIVES:
    The aim of the present study was to investigate the effects of nicotine on the expression of HO-1 protein in cultured human gingival fibroblasts in vitro and further to compare HO-1 expression in gingival tissues obtained from cigarette smokers and non-smokers in vivo.
    METHODS:
    Western blot assay was used to investigate the effects on human gingival fibroblasts exposed to nicotine. In addition, antioxidants catalase, superoxide dismutase (SOD), and N-acetyl-l-cysteine (NAC) were added to test how they modulated the effects on nicotine-induced HO-1 expression. Gingival biopsies taken from the flap surgery of 20 male patients with periodontal disease (10 cigarette smokers and 10 non-smokers) were examined by immunohistochemistry.
    RESULTS:
    The exposure of quiescent human gingival fibroblasts to 10 mm nicotine resulted in the induction of HO-1 protein expression in a time-dependent manner (p < 0.05). The addition of glutathione (GSH) precursor NAC inhibited the nicotine-induced HO-1 protein expression (p < 0.05). However, SOD and catalase did not decrease the nicotine-induced HO-1 protein expression (p > 0.05). The results from immunohistochemistry demonstrated that HO-1 expression was significantly higher in cigarette smokers (p < 0.05). HO-1 was noted in the basal layers of epithelium, inflammatory cells, and fibroblasts in specimens from cigarette smoking.
    CONCLUSIONS:
    Taken together, these results suggest that HO-1 expression is significantly up-regulated in gingival tissues from cigarette smokers, and nicotine may, among other constituents, be responsible for the enhanced HO-1 expression in vivo. The regulation of HO-1 expression induced by nicotine is critically dependent on the intracellular GSH concentration.
    URI: https://ir.csmu.edu.tw:8080/ir/handle/310902500/11342
    http://dx.doi.org/10.1111/j.1600-0765.2005.00804.x
    關聯: J Periodontal Res. 2005 Jun;40(3):252-7.
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