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托珠单抗治疗的类风湿关节炎患者血清氧化应激标志物水平显著降低。

Serum level of oxidative stress marker is dramatically low in patients with rheumatoid arthritis treated with tocilizumab.

机构信息

Department of Orthopaedics, Osaka University Graduate School of Medicine, Osaka, Japan.

出版信息

Rheumatol Int. 2012 Dec;32(12):4041-5. doi: 10.1007/s00296-011-2135-0. Epub 2011 Sep 11.

Abstract

Regarding the pathobiology of rheumatoid arthritis, oxidative stress induced by reactive oxygen species is an important mechanism that underlies destructive and proliferative synovitis. Abundant amounts of reactive oxygen species have been detected in the synovial fluid of inflamed rheumatoid joints. It is reported that drugs that block tumor necrosis factor-α reduce the oxidative stress marker levels in patients with rheumatoid arthritis. In this study, we measured reactive oxygen species using a free radical analytical system in patients with rheumatoid arthritis treated with disease-modifying antirheumatic drugs, tumor necrosis factor-α-blocking drugs (infliximab, etanercept), and an interleukin-6-blocking drug (tocilizumab). The serum level of oxidative stress was drastically low in patients with rheumatoid arthritis treated with tocilizumab, suggesting that interleukin-6 blocking therapy reduces not only joint damage, but also vascular degeneration in patients with rheumatoid arthritis. We believe that such a drastic effect would reduce the incidence of cardiovascular events and mortality in patients with rheumatoid arthritis.

摘要

关于类风湿关节炎的发病机制,活性氧诱导的氧化应激是导致破坏性和增殖性滑膜炎的重要机制。在炎症性类风湿关节的滑液中检测到大量的活性氧。据报道,阻断肿瘤坏死因子-α的药物可降低类风湿关节炎患者的氧化应激标志物水平。在这项研究中,我们使用自由基分析系统测量了类风湿关节炎患者在使用疾病修饰抗风湿药物、肿瘤坏死因子-α阻断药物(英夫利昔单抗、依那西普)和白细胞介素-6 阻断药物(托珠单抗)治疗后的活性氧水平。接受托珠单抗治疗的类风湿关节炎患者的血清氧化应激水平显著降低,表明白细胞介素-6 阻断疗法不仅可减轻关节损伤,还可减轻类风湿关节炎患者的血管退化。我们认为,这种显著的效果可降低类风湿关节炎患者发生心血管事件和死亡的风险。

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