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目的 检测系统性红斑狼疮 (SLE)患者谷胱甘肽转移酶 μ(GSTμ)基因缺失及血中一氧化氮 (NO)、脂质过氧化物 (LPO)、超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH Px)和谷胱甘肽 (GSH)含量 ,分析其与SLE发病之间的关系。方法 用PCR法检测 87例SLE患者和 40名健康对照组的GSTμ基因 ,用化学分析法测上述 5项指标。 结果 SLE患者GSTμ基因缺失率达 6 9 0 % ,明显高于对照组的 47 5 %。SLE活动期NO(79± 18) μmol/L、LPO (10 4± 2 0 ) μmol/L明显高于稳定期和对照组的水平。SLE活动期SOD (12 86± 2 5 2 ) μU/L、GSH Px (78± 14)U/mg、GSH (0 37±0 0 5 )mg/ g明显低于稳定期及对照组水平。在SLE稳定期GSH (1 0 0± 0 14)mg/ g ,仍明显低于对照组水平。血清NO水平与LPO呈显著直线正相关 ,与SOD、GSH Px、GSH呈显著直线负相关。抗dsDNA与NO、LPO呈显著直线正相关。在SLE活动期 ,GSTμ基因缺失者LPO (11 4± 2 2 ) μmol/L明显高于GSTμ基因携带者的水平 ,SOD (1111± 2 18) μU/L、GSH Px (6 7± 14)U/mg、GSH (0 2 4±0 0 4)mg/g明显低于GSTμ基因携带者的水平。在SLE稳定期GSTμ基因缺失者的SOD和GSH水平仍低于GSTμ基因携带者。 结论 GSTμ基因缺失可能是SLE发病的遗传因素之一 ,SLE?
Objective To detect the gene deletion of glutathione transferase μ (GSTμ) and the levels of blood nitric oxide (NO), lipid peroxidation (LPO) and superoxide dismutase (SOD) in patients with systemic lupus erythematosus (SLE) Glutathione peroxidase (GSH Px) and glutathione (GSH) content, analysis of its relationship with the pathogenesis of SLE. Methods PCR was used to detect the GSTμ gene in 87 patients with SLE and 40 healthy controls. The above five indexes were determined by chemical analysis. Results The deletion rate of GSTμ gene in SLE patients was 69.0%, which was significantly higher than 47.5% in control group. NO (79 ± 18) μmol / L and LPO (104 ± 2 0) μmol / L in active SLE group were significantly higher than those in stable group and control group. The activities of SLE during the active phase (12 86 ± 2 5 2 μU / L, GSH Px (78 ± 14) U / mg and GSH (0 37 ± 0 0 5) mg / g were significantly lower than those of the control group and the stationary phase. In the stable phase of SLE GSH (100 ± 0 14) mg / g, still significantly lower than the control group. There was a significant linear positive correlation between serum NO level and LPO and a significant linear negative correlation with serum SOD, GSH Px and GSH. There was a significant linear positive correlation between anti-dsDNA and NO and LPO. LPO (11 4 ± 2 2) μmol / L in GSTμ gene deletion group was significantly higher than that in GSTμ gene carrier group (1111 ± 2 18 μU / L, GSH Px (6 7 ± 14) U / mg, GSH (0 24 ± 0 0 4) mg / g was significantly lower than that of GSTμ gene carriers. The levels of SOD and GSH in GSTμ gene-deficient subjects were still lower than those of GSTμ gene in stable SLE patients. Conclusion GSTμ gene deletion may be one of the genetic factors in the pathogenesis of SLE. SLE?