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骨关节炎患者滑膜细胞中脂质过氧化作用增强。

Enhanced lipid peroxidation in synoviocytes from patients with osteoarthritis.

作者信息

Grigolo Brunella, Roseti Livia, Fiorini Mauro, Facchini Andrea

机构信息

Laboratorio di Immunologia e Genetica, Istituto di Ricerca Codivilla Putti, Bologna, Italy.

出版信息

J Rheumatol. 2003 Feb;30(2):345-7.

Abstract

OBJECTIVE

To evaluate the degree of lipid peroxidation of synoviocytes from patients with rheumatoid arthritis (RA), osteoarthitis (OA), and controls and to look at the production of nitric oxide (NO) and its involvement in this process.

METHODS

Human synoviocytes were isolated from synovial tissues from patients with RA, OA, and from healthy controls. Cells were maintained in culture for up to 3 culture passages. Lipid peroxidation, verified by the production of malonaldehyde (MDA) and 4-hydroxy-2(E)-nonenal (4-HNE), was determined by colorimetric assay. NO was evaluated by estimating the stable NO metabolite nitrite by the Griess method in the supernatants of unstimulated and interleukin (IL)-1beta and tumor necrosis factor (TNF)-a stimulated cells.

RESULTS

Increased levels of lipid peroxidation were observed for OA-derived synoviocytes compared to RA and controls. The cells in each experimental group produced low amounts of NO both in basal and in stimulated conditions.

CONCLUSION

In OA, synovial cells underwent a lipid peroxidation process that did not occur in synoviocytes from RA or controls even in the absence of a detectable production of the reactive nitrogen intermediate NO. We can postulate that this peroxidation process might be due to the action of NO secreted by chondrocytes that are known to produce higher levels of this radical in OA compared to RA.

摘要

目的

评估类风湿关节炎(RA)、骨关节炎(OA)患者及对照者滑膜细胞的脂质过氧化程度,并观察一氧化氮(NO)的产生及其在此过程中的作用。

方法

从RA、OA患者及健康对照者的滑膜组织中分离人滑膜细胞。细胞在培养中传代培养多达3代。通过比色法测定由丙二醛(MDA)和4-羟基-2(E)-壬烯醛(4-HNE)生成所验证的脂质过氧化。通过Griess法在未刺激以及白细胞介素(IL)-1β和肿瘤坏死因子(TNF)-α刺激的细胞上清液中估计稳定的NO代谢产物亚硝酸盐来评估NO。

结果

与RA和对照相比,OA来源的滑膜细胞脂质过氧化水平升高。每个实验组的细胞在基础状态和刺激状态下均产生少量NO。

结论

在OA中,滑膜细胞经历了脂质过氧化过程,而RA或对照的滑膜细胞即使在未检测到活性氮中间体NO产生的情况下也未发生这种过程。我们可以推测,这种过氧化过程可能是由于软骨细胞分泌的NO的作用,已知与RA相比,OA中的软骨细胞产生更高水平的这种自由基。

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