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甲硫醇对人牙龈成纤维细胞和单核细胞培养物中酶及细胞因子产生的刺激作用。

Stimulation of enzyme and cytokine production by methyl mercaptan in human gingival fibroblast and monocyte cell cultures.

作者信息

Ratkay L G, Waterfield J D, Tonzetich J

机构信息

Department of Oral Biology, Faculty of Dentistry, University of British Columbia, Vancouver, Canada.

出版信息

Arch Oral Biol. 1995 Apr;40(4):337-44. doi: 10.1016/0003-9969(94)00165-8.

DOI:10.1016/0003-9969(94)00165-8
PMID:7605261
Abstract

The volatile sulphur compound methyl mercaptan (CH3SH) is a by-product of protein metabolism and a principal component of oral malodour. This investigation examines the effect of CH3SH on the enzymatic activities of cathepsins B and G and elastase, and on the production by human gingival fibroblasts of two key factors, prostaglandin E (PGE) and cAMP, of the PGE2-cAMP-dependent pathway, which may contribute to the increased production of collagenase and tissue destruction in human periodontal disease. The results demonstrate that CH3SH alone, or in combination with interleukin-1 (IL-1) or lipopolysaccharide, can significantly enhance the secretion of PGE2, cAMP and procollagenase by human gingival fibroblasts. CH3SH also stimulated mononuclear cells to produce IL-1, which can increase cAMP production, and act in synergism with the direct effect of CH3SH on cAMP. CH3SH also significantly enhanced the activity of cathepsin B, moderately suppressed that of cathepsin G, but did not significantly affect elastase. These results provide evidence that CH3SH could be a contributing factor in the enzymatic and immunological cascade of events leading to tissue degradation in periodontal diseases.

摘要

挥发性硫化合物甲硫醇(CH3SH)是蛋白质代谢的副产物,也是口腔异味的主要成分。本研究考察了CH3SH对组织蛋白酶B和G以及弹性蛋白酶的酶活性的影响,以及对人牙龈成纤维细胞产生前列腺素E(PGE)和环磷酸腺苷(cAMP)这两种PGE2 - cAMP依赖性途径关键因子的影响,这可能导致人类牙周病中胶原酶产生增加和组织破坏。结果表明,单独的CH3SH,或与白细胞介素 - 1(IL - 1)或脂多糖联合使用,均可显著增强人牙龈成纤维细胞分泌PGE2、cAMP和前胶原酶。CH3SH还刺激单核细胞产生IL - 1,IL - 1可增加cAMP的产生,并与CH3SH对cAMP的直接作用协同发挥作用。CH3SH还显著增强了组织蛋白酶B的活性,适度抑制了组织蛋白酶G的活性,但对弹性蛋白酶没有显著影响。这些结果证明,CH3SH可能是导致牙周病组织降解的酶促和免疫级联反应中的一个促成因素。

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