Mititelu Radu Răzvan, Pădureanu Rodica, Băcănoiu Manuela, Pădureanu Vlad, Docea Anca Oana, Calina Daniela, Barbulescu Andreea Lili, Buga Ana Maria
Department of Biochemistry, University of Medicine and Pharmacy of Craiova, 200349 Craiova, Romania.
Department of Physical Therapy and Sports Medicine, University of Craiova, 200207 Craiova, Romania.
Biomedicines. 2020 May 15;8(5):125. doi: 10.3390/biomedicines8050125.
Rheumatoid arthritis (RA) is a chronic progressive autoimmune disease, associated with significant morbidity, mainly due to progressive damage and consequent disability. Oxidative stress is an important part of RA pathophysiology, as in autoimmune disease the interaction between immune response and endogenous/exogenous antigens subsequently induce the production of reactive oxygen species. The oxidative stress process seems to be positively strongly correlated with inflammation and accelerated joint destruction. We were asking ourselves if the oxidative stress biomarkers are the mirror tools of disease activity, outcome, and inflammation level in a group of RA patients under standard or biological therapy compared to healthy age-matched controls. In order to do this, the oxidative stress damage biomarkers (lipids peroxide and protein carbonyl level), antioxidant defense capacity, and pro-inflammatory status of plasma were quantified. In this study, we took into account the complete picture of RA diseases and assessed, for the first time, the inflammatory level in correlation with the oxidative stress level and antioxidant capacity of RA patients. Our results revealed that protein oxidation through carbonylation is significantly increased in RA groups compared to controls, and both protein carbonyl Pcarb and thiobarbituric acid reactive substance (TBARS) are reliable markers of ROS damage. Therefore, it is unanimous that neutrophil/lymphocyte ratio (NLR), monocyte/lymphocyte ratio ( MLR), platelet/lymphocyte ratio (PltLR) correlated with Pcarb, and TBARS can provide a view of the complex phenomenon represented by proteins/lipids damage, key contributors to disease outcome, and an increased awareness should be attributed to these biomarkers.
类风湿关节炎(RA)是一种慢性进行性自身免疫性疾病,会导致严重的发病情况,主要是由于进行性损伤及随之而来的残疾。氧化应激是RA病理生理学的重要组成部分,因为在自身免疫性疾病中,免疫反应与内源性/外源性抗原之间的相互作用随后会诱导活性氧的产生。氧化应激过程似乎与炎症和加速的关节破坏呈正相关。我们一直在思考,与年龄匹配的健康对照相比,氧化应激生物标志物是否是一组接受标准治疗或生物治疗的RA患者疾病活动、预后及炎症水平的反映指标。为了做到这一点,我们对氧化应激损伤生物标志物(过氧化脂质和蛋白质羰基水平)、抗氧化防御能力以及血浆的促炎状态进行了量化。在本研究中,我们综合考虑了RA疾病的全貌,并首次评估了RA患者炎症水平与氧化应激水平及抗氧化能力的相关性。我们的结果显示,与对照组相比,RA组中通过羰基化作用导致的蛋白质氧化显著增加,并且蛋白质羰基(Pcarb)和硫代巴比妥酸反应性物质(TBARS)都是活性氧损伤的可靠标志物。因此,一致认为中性粒细胞/淋巴细胞比率(NLR)、单核细胞/淋巴细胞比率(MLR)、血小板/淋巴细胞比率(PltLR)与Pcarb相关,并且TBARS可以反映由蛋白质/脂质损伤所代表的复杂现象,而蛋白质/脂质损伤是疾病预后的关键因素,应该更多地关注这些生物标志物。