Rheumatoid arthritis is prevalent in more than 1% of the global population, with the highest occurrence between ages 35 and 50, which places a huge burden on the economy. Drug discovery for the prevention of this chronic disease is; therefore, a priority. It is known that subclinical progression of many chronic non-communicable diseases is exacerbated via accelerated ageing, a pro-inflammatory phenotype shift. However, rheumatoid arthritis additionally has significant humoral immune activation, inflammatory signalling—and thus the accelerated ageing profile—may differ from other chronic inflammatory diseases. The current study simulated inflammatory arthritis onset in a collagen-induced arthritis (CIA) rodent model, to characterise the redox and inflammatory profile at the onset of clinical symptoms, in different tissues, in the presence and absence of preventative antioxidant treatment. The data illustrate that an increased free radical level are evident already very early on in RA disease progression. Furthermore, oxidative stress seems to somewhat precede a significant pro-inflammatory state, perhaps due to humoral immune activation. Our data across different compartments further suggest that the compensatory increase in endogenous antioxidant activity is gradually exhausted at a different pace, with the liver showing the first signs of oxidant damage, even before significant evidence exist in circulation. The current data further suggest that preventative antioxidant intervention may have a sparing effect on endogenous antioxidant mechanisms and preserve telomere length to delay disease progression—or at least the accelerated ageing known to exacerbate RA symptoms—although it did not seem to have a significant direct effect on the autoimmune activity.

中文翻译：

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炎性关节炎的加速衰老过程是独特的，并且是组织区室特异性的。

类风湿关节炎在全球超过1％的人口中普遍存在，在35岁至50岁之间发病率最高，给经济带来了沉重负担。预防这种慢性疾病的药物发现是；因此，优先考虑。众所周知，许多慢性非传染性疾病的亚临床进展会通过加速衰老，促炎性表型转变而加剧。然而，类风湿关节炎还具有显着的体液免疫激活，炎症信号传导-从而加速了衰老过程-可能与其他慢性炎症性疾病有所不同。当前的研究在胶原蛋白诱导的关节炎（CIA）啮齿动物模型中模拟了炎症性关节炎的发作，以表征不同组织中临床症状发作时的氧化还原和炎症状况，在有和没有预防性抗氧化剂治疗的情况下。数据表明，自由基水平升高已在RA疾病发展的很早阶段就显现出来。此外，氧化应激似乎在某种程度上早于明显的促炎状态，这可能是由于体液免疫激活所致。我们跨不同区室的数据进一步表明，内源性抗氧化剂活性的补偿性增加以不同的速度逐渐耗尽，即使在循环中没有明显证据存在之前，肝脏也显示出氧化损伤的最初迹象。