谷胱甘肽转移酶μ基因缺失和氧化损伤与系统性红斑狼疮相关性研究

Relationship between the glutathione S-transferase class μ (GSTμ) gene deletion,oxidative injury and systemic lupus erythematosus

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 determine the glutathione S transferase class μ (GSTμ) gene and the level of nitric oxide (NO),lipid peroxide (LPO),superoxide dismutase (SOD),glutathione peroxidase (GSH Px) and glutathione (GSH) of patients with systemic lupus erythematosus (SLE) and analyse the relationship between them and SLE.Methods GSTμ gene of 87 SLE patients and 40 healthy subjects were determined by PCR method.NO,LPO,SOD,GSH Px and GSH were determined by chemical analysis methods.Results The rate of GSTμ gene deletion in patients with SLE was 69 0%,which was significantly higher than that of the controls (47 5%).The levels of NO (79±18) μmol/L and LPO (10 4±2 0) μmol/L of active SLE group were higher than those of stable SLE group [NO (55±12) μmol/L,LPO (6 9±1 6) μmol/L] and healthy group [NO (50±9) μmol/L,LPO (5 7±1 4) μmol/L].The levels of SOD (1 286±252) μU/L,GSH Px (78±14) U/mg and GSH (0 37±0 05) mg/g of active SLE group were lower than those of stable SLE group [SOD (1 866±381) μU/L,GSH Px (138±19) U/mg,GSH (1 00±0 14) mg/g] and healthy group [SOD (2 065±375) μU/L,GSH Px (143±29) U/mg,GSH (1 28±0 19) mg/g].The level of GSH (1 00±0 14) mg/g of stable SLE group was lower than that of healthy group [(1 28±0 19) mg/g].The obvious positive correlation was observed between serum NO and LPO ( r =0 717, P <0 01).The obvious negative correlations were observed between NO and SOD,GSH Px,GSH ( r =-0 747,-0 766,-0 707, P <0 01).The obvious positive correlations were observed between anti dsDNA and NO,LPO ( r =0 718,0 713, P <0 01).The obvious negative correlations were observed between anti dsDNA and SOD,GSH Px,GSH ( r =-0 583, -0 745, -0 698, P <0 01).In active SLE group,the level of LPO (11 4±2 2) μmol/L of GSTμ gene deletion was higher than that of GSTμ gene carriers (9 3±1 8) μmol/L,the levels of GSTμ gene deletion were lower than those of GSTμ gene carriers [SOD (1 547±296) μU/L,GSH Px (104±15) U/mg,GSH (0 66±0 06) mg/g].In stable SLE group,the levels of SOD [(1 760±352) μU/L] and GSH[(0 86±0 15) mg/g] of GSTμ gene deletion were lower than those of GSTμ gene carriers [SOD (2 122±407) μU/L,GSH (1 35±0 12) mg/g].Conclusion GSTμ gent deletion may play an important role in etiopathology of SLE.There is oxidative injury in active SLE.The oxidative injury in cases of GSTμ gene deletion was more serious than that of GSTμ gene carriers.