中文摘要：

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.

英文摘要：

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.