Henrotin Y E, Zheng S X, Deby G P, Labasse A H, Crielaard J M, Reginster J Y
Bone and Cartilage Metabolism Research Unit, Institute of Pathology, University of Liège, Belgium.
J Rheumatol. 1998 Aug;25(8):1595-601.
To investigate the effects of endogenously produced nitric oxide (NO) on interleukin 6 (IL-6), IL-8, prostaglandin E2 (PGE2), and proteoglycan production by human chondrocytes.
Human articular chondrocytes were isolated from their extracellular matrix by triple successive enzymatic digestion of the cartilage and cultured 48 h in a well defined culture medium. IL-6 and IL-8 were directly assayed into culture media by specific enzyme amplified sensitivity immunoassays. Proteoglycans and PGE2 were quantified by specific radioimmunoassays. Cell culture media were assayed for NO2 using a spectrophotometric assay based upon the Griess reaction.
Unstimulated chondrocytes produced low levels of NO, IL-6, IL-8, and PGE2. Production was significantly stimulated by IL-1beta and lipopolysaccharide (LPS). As well, proteoglycan synthesis was profoundly inhibited by IL-1beta and LPS. Inhibition of NO synthesis with the competitive inhibitor NG-monomethyl-L-arginine (L-NMMA) led to enhancement of IL-6, IL-8, and PGE2 production stimulated by either IL-1beta alone or in combination with LPS, whereas the inhibition of proteoglycan production by IL-1beta was not modified by L-NMMA.
LPS and IL-1beta stimulated IL-6, IL-8, and PGE2 production are downregulated by endogenously produced NO, which could limit the inflammatory reaction occurring in arthritis.
研究内源性一氧化氮（NO）对人软骨细胞白细胞介素6（IL-6）、IL-8、前列腺素E2（PGE2）和蛋白聚糖产生的影响。
通过对软骨进行连续三次酶消化从细胞外基质中分离出人关节软骨细胞，并在明确的培养基中培养48小时。通过特异性酶放大灵敏度免疫测定法直接检测培养基中的IL-6和IL-8。通过特异性放射免疫测定法定量蛋白聚糖和PGE2。使用基于格里斯反应的分光光度法检测细胞培养基中的NO2。
未受刺激的软骨细胞产生低水平的NO、IL-6、IL-8和PGE2。IL-1β和脂多糖（LPS）可显著刺激其产生。同样，IL-1β和LPS可深刻抑制蛋白聚糖的合成。用竞争性抑制剂NG-单甲基-L-精氨酸（L-NMMA）抑制NO合成导致单独或与LPS联合使用的IL-1β刺激的IL-6、IL-8和PGE2产生增加，而L-NMMA未改变IL-1β对蛋白聚糖产生的抑制作用。
内源性产生的NO可下调LPS和IL-1β刺激的IL-6、IL-8和PGE2产生，这可能限制关节炎中发生的炎症反应。
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