蛋白质氧化损伤与系统性红斑狼疮疾病活动的相关性研究

Study on the relationship between protein oxidation and disease activity in systemic lupus erythematosus

目的探讨系统性红斑狼疮（SLE）患者蛋白质氧化损伤程度与疾病活动的关联。方法收集SLE患者临床资料，采用病例对照研究，应用分光光度法测定蛋白质羰基、巯基、超氧化物歧化酶（SOD）、髓过氧化酶（MPO）和总抗氧化能力（TAOC）等蛋白质氧化损伤相关指标，ELISA法定性测定血浆抗-dsDNA抗体和抗核抗体的水平。结果SLE患者蛋白质氧化程度与健康对照组的差异有统计学意义，蛋白质羰基浓度升高[（0101±0．033）nmol／mg、（0．061±0．019）nmol／mg，P〈0．01]，蛋白质巯基浓度[（3．911±0．968）nmol／mg、（4．655±0．798）nmol／mg，P〈0．01]和T-SOD[（67．01±12．22）U／ml、（97．35±14．11）U／ml，P〈0．01]浓度降低，且与疾病活动相关指标有一定关联。抗-dsDNA抗体阳性组血浆蛋白质巯基浓度、T-SOD活性低于阴性组，差异有统计学意义。结论处于疾病活动状态的SLE患者，存在一定程度的蛋白质过氧化现象。且氧化损伤程度与疾病活动正相关，提示蛋白质氧化对于SLE慢性器官损伤的发病机制是否有一定作用值得进一步研究。

Objective To examine the levels of protein oxidation in systemic lupus erythematosus （SLE） and to evaluate the relation between oxidative protein damage and disease activity index. Methods Plasma was collected from SLE patients and healthy subjects as controls. Protein-bound carbonyls, protein thiols, superoxide dismutase （SOD）, myeloperoxidase （MPO） and total antioxidant capacity （TAOC） were determined by spectrophotometry. Levels of anti-double-stranded DNA （anti-dsDNA） and antinuclear antibody （ANA） were quantified by enzyme-linked immunosorbent assay. Results When comparing with the control subjects, SLE patients exhibited elevated levels of protein carbonyls [（0.101 ±0.033 ） nmol/mg, （ 0. 061± 0. 019 ） nmol/mg, P 〈 0.01 ], degraded levels of protein thiols [ （ 3. 911± 0. 968 ） nmol/mg,（4.655±0.798） nmol/mg, P〈 0. 01] and activities of T-SOD [（67.01±12.22） U/ml, （97.35± 14.11 ）U/ml, P 〈 0.01 ]. Levels of plasma protein thiols and activities of T-SOD were lower in SLE patients positive for anti-dsDNA antibody, compared with patients negative for anti-dsDNA antibody. Conclusion We found that the elevated levels of multiple markers of protein oxidation and degraded activities of antioxidant enzymes in plasma from SLE patients existed when comparing with the controls, and the all the levels were correlated with disease activity. Our findings suggested that protein oxidation might play a role in the pathogenesis of chronic organ damage in SLE.