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一氧化氮与软骨损伤

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关键词: 一氧化氮(NO),软骨破坏

一氧化氮(NO)在不同的生物系统中充当调节和效应因子〔1~5〕,如作为神经递质在神经系统中发挥作用,松驰平滑肌,抑制血小板聚集,介导细胞增殖抑制和非特异抗微生物防御反应。近来研究发现NO参与软骨破坏的病理过程。
  NO由一氧化氮合酶(NOS)催化L-精氨酸产生,需要烟酰胺腺嘌呤二核苷酸(NAPDH)、四氢叶酸和分子氧作为辅助因子〔6〕。新生成的NO在局部激活鸟苷酸环化酶,升高细胞内cGMP水平,发挥生物学效应〔7〕。NOS按表达方式分为自发型(包括神经型和内皮型)和诱导型(iNOS)两种,两种酶在多种细胞中共同存在,但相对水平不同。自发型需要Ca2+/Ca2+通道参与〔8〕,蛋白激酶C(PKC)、cAMP依赖蛋白激酶(PKA)等通过磷酸化NOS调节其活性〔9〕。自发型仅产生少量NO。而诱导型在细胞因子如白细胞介素-1(IL-1)、肿瘤坏死因子(TNF)等和脂多糖(LPS)刺激数小时后即产生大量NO,其活性依赖于mRNA的产生和蛋白表达,与Ca2+/Ca2+通道无关。iNOS在不同细胞中的质和量不同,在人肝细胞中NO的诱导需要IL-1、TNF、LPS和干扰素(IFN)联合刺激,而IL-1单独刺激血管平滑肌细胞产生NO。软骨细胞在IL-1、LPS和TNF单独刺激下产生大量NO,作用具有协同性〔10〕。
  编码人软骨细胞iNOS的cDNA已被克隆,是一条4.5kb的单链,编码一条1153个氨基酸序列的长链蛋白〔11〕。与鼠巨噬细胞iNOS相比,cDNA具有78%同源性,蛋白质具有88%同源性。与鼠巨噬细胞NOS相比,同源性较低。iNOS和NOS都有黄素腺嘌呤二核苷酸(FAD)、黄素单核苷酸(FMN)、NAPDH和钙通道结合位点。糖皮质激素和非甾体抗炎药在其他细胞能抑制iNOS的表达,但对软骨细胞iNOS的表达无影响〔12〕。有资料报道软骨细胞内Ca2+浓度升高可减少iNOS mRNA的稳定性,软骨细胞iNOS是一种钙依赖的新型合酶〔13〕。PKC、PKA等与软骨细胞iNOS活性无关,而酪氨酸激酶(PTK)激活可以促进软骨细胞iNOS mRNA产生和蛋白表达〔14〕。
目录:
  1 NO抑制软骨细胞增殖,诱导软骨细胞凋亡

  2 NO对蛋白聚糖(PG)代谢的影响

  3 NO促进MMPs的产生


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