变应性鼻炎患者血清氧化应激状态研究

目的 检测变应性鼻炎(allergic rhinitis,AR)患者外周血血清中氧化应激标志物,探讨氧化应激反应在AR发病机制中的作用.方法 留取23例健康人、48例AR患者外周血血清,分别检测氧化应激标志物一氧化氮(nitric oxide,NO)、诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)、总一氧化氮合酶(total nitric oxide synthase,TNOS),脂质过氧化产物丙二醛(malondidehyde,MDA),以及体内主要抗氧化酶超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)水平.采用SPSS 13.0软件对数据进行分析.结果 AR患者血清NO水平((x)±s,以下同)为(97.92±73.42)μmol/L]较健康对照组(64.04±29.54)μmol/L]明显升高(t=-0.281,P<0.05);iNOS与TNOS比值(0.51±0.11)较健康对照组(0.45±0.15)明显升高(t=-2.061,P<0.05);血清GSH-Px活性(258.24±45.25)U/(ml·min)]较健康对照组(215.11±47.62)U/(ml·min)]明显升高(t=-2.2349,P<0.05)).而AR患者血清SOD活性、MDA含量较健康对照组分别有升高和降低趋势,但差异无统计学意义(Z=-1.656,t=1.922,P值均>0.05).结论 氧化应激反应参与AR病理生理过程,而iNOS-NO通路在AR的发病过程中可能发挥着更为重要的作用.

Changes of oxidative stress in peripheral serum of patients with allergic rhinitis

Objective To examine the changes of oxidative stress biomarkers in peripheral serum of patients with allergic rhinitis (AR) , so as to investigate the role of oxidative stress in pathogenesis of AR. Methods The levels of serum nitric oxide (NO), malondidehyde (MDA) , as well as the activities of serum nitric oxide synthase (NOS), antioxidant enzymes including superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured in 48 AR patients and 23 healthy controls. Statistical analysis was performed using a SPSS 13. 0 software. Results The level of serum NO in AR group (97. 92 ±73.42) μmol/L] was higher than that in healthy control group (64. 04 ± 29. 54) μmol/L] , the diference was significant (t = -0. 281, P <0.05). The ratio of inducible NOS (iNOS) to total NOS (TNOS) in AR group (0.51 ±0. 11) was higher than that in healthy control group (0.45 ±0. 15), the diference was significant (t = - 2.061, P < 0.05 ) . The activity of serum GSH-Px in AR group (258. 24 ±45.25) U/(ml ·min) ] was higher than that in healthy control group(215. 11 ±47.62) U/( ml ·min) ] , the diference was significant (t = - 2. 235, P < 0. 05 ). Although activity of SOD, concentration of MDA in AR group had a tendency to increase and decrease, respectively, no significant statistical difference was found as compared to the control group(P >0. 05). Conclusion Oxidative stress is involved in the pathophysiology of AR, however, iNOS-NO pathway may play a more important role in AR pathogenesis.