Antioxidant Enzymes in Rheumatoid Arthritis

Vivek Kumar, J. Prakash, Varsha Gupta, M. Y. Khan
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引用次数: 9

Abstract

Joint destruction in rheumatoid arthritis (RA) is due to tissue injury in the area caused by inflammatory reactions, release of MMPs and free radicals produced by neutrophils and macrophages. The control of free radical production may have therapeutic roles thus the study was done to check the status of lipid peroxidation product malondialdehyde (MDA) and a few antioxidant enzymes in RA patients. 45 RA patients and 40 controls were selected. Controls were asymptomatic and RA patients were selected according to ACR criteria. RA patients had significantly high MDA, SOD and ALP and reduced activity of catalase and GR as compared to controls. SOD showed positive correlation with ALP. GR was positively related with MDA, SOD and ALP. The study shows that MDA is involved in the pathogenesis of RA. The system is trying to quench free radicals by high SOD activity. Higher production of H2O2 or some other mechanism is responsible for inhibition of catalase and GR. However system is trying to reduce the damage by neutralizing superoxide anion. Therapeutic intervention of the oxidative stress may be considered for effective control of inflammation in RA patients.
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类风湿关节炎中的抗氧化酶
类风湿性关节炎(RA)的关节破坏是由于炎症反应、中性粒细胞和巨噬细胞产生的MMPs和自由基的释放引起的区域组织损伤。控制自由基的产生可能具有治疗作用,因此研究了RA患者脂质过氧化产物丙二醛(MDA)和几种抗氧化酶的状态。选取RA患者45例,对照组40例。对照组无症状,根据ACR标准选择RA患者。与对照组相比,RA患者的MDA、SOD和ALP明显升高,过氧化氢酶和GR活性降低。SOD与ALP呈正相关。GR与MDA、SOD、ALP呈正相关。研究表明MDA参与了RA的发病过程。系统正试图通过高SOD活性来抑制自由基。过氧化氢酶和GR的抑制是由H2O2的产生或其他机制引起的,但系统正试图通过中和超氧阴离子来减少损伤。治疗性干预氧化应激可考虑有效控制RA患者的炎症。
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