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氧化应激失衡在支气管哮喘急性发作中的意义
引用本文:马南,耑冰,李萍,苑群,汪涛,杨朝.氧化应激失衡在支气管哮喘急性发作中的意义[J].中华全科医学,2019,17(12):1993-1997.
作者姓名:马南  耑冰  李萍  苑群  汪涛  杨朝
作者单位:1. 滨州市人民医院呼吸内科, 山东 滨州 256610;
基金项目:国家自然科学基金(81160011,81560014,81470252);宁夏回族自治区2017年度留学人员创新创业项目(宁人社函〔2017〕84号);宁夏回族自治区2018年度重点研发计划一般项目(2018BEG03052,2018BEG03054)
摘    要:目的 观察支气管哮喘急性发作期患者血清活性氧(ROS)、8-羟基脱氧鸟苷(8-OHdG)、蛋白质羰基(PC)、丙二醛(MDA)和核因子κB(NF-κB)及硫化氢(H2S)、总抗氧化能力(T-AOC)水平及意义。 方法 选取宁夏回族自治区人民医院2016年10月—2017年3月60例哮喘急性发作期患者,分为治疗前(A)组(又分轻度组和中-重度组)和治疗后(B)组,60例健康体检者为对照(C)组,用ELISA等方法检测并分析。 结果 ①A、B、C组ROS、8-OHdG、PC、MDA及NF-κB逐渐降低;H2S和T-AOC逐渐升高(均P<0.05)。②中重度组较轻度组ROS、PC、MDA及NF-κB明显升高;H2S、T-AOC明显降低(均P<0.05)。③ROS、PC、MDA、NF-κB与T-AOC、FEV1%pred及ACT评分呈负相关;H2S与T-AOC、FEV1%pred及ACT评分呈正相关(均P<0.05)。④PC、MDA受ROS影响(均P<0.05),MDA受ROS影响比PC大(β=0.411)。 结论 氧化应激失衡参与了哮喘的发病,ROS可能通过NF-κB引起蛋白及脂质过氧化而对机体产生损伤,H2S可能通过抑制ROS及NF-κB而发挥抗氧化作用;ROS、PC及MDA可作为哮喘严重程度及控制水平的监测指标,内源性H2S可能成为哮喘潜在的治疗靶点。 

关 键 词:支气管哮喘    氧化应激    活性氧    蛋白质羰基    丙二醛    核因子kappaB    内源性硫化氢
收稿时间:2019-01-26

Significance of oxidative stress in acute exacerbation of bronchial asthma
Affiliation:Department of Respiratory Medicine, Binzhou People's Hospital, Binzhou, Shandong 256610, China
Abstract:Objective To observe predictive significance of serum reactive oxygen species (ROS), 8-hydroxydeoxyguanosine (8-OHdG), protein carbonyls (PC), malondialdehyde (MDA), nuclear factor of kappaB (NF-κB), hydrogen sulfide (H2S), total antioxidant capacity (T-AOC) in patients with acute exacerbation of bronchial asthma. Methods Sixty patients with bronchial asthma acute exacerbation and 60 healthy individuals in Ningxia Hui Autonomous Region People's Hospital between October 2016 to March 2017 were recruited in the study. The patients were assigned into pre-treatment (A) group (further into the mild subgroup and the moderate-severity subgroup according to the severity) and post-treatment (B) group according to treatment. Sixty healthy individuals were set as control (C) group. The serum levels of ROS, 8-OHdG, PC, MDA, NF-κB, H2S and T-AOC were tested with ELISA. The pulmonary function (FEV1%pred) and asthma control test (ACT) were measured. Results ① The levels of ROS, 8-OHdG, PC, MDA and NF-κB in group C were lower than those in group B, and then group A; The levels of H2S and T-AOC were higher in group C than group B, and then group A, the difference was significant (all P<0.05). ② The levels of ROS, PC, MDA and NF-κB in the moderate to severe group were significantly higher than those in the mild group; However, the levels of H2S and T-AOC in the moderate to severe group were significantly lower as compared with the mild group (all P<0.05). ③ The serum levels of ROS, PC, MDA and NF-κB were negatively correlated with T-AOC, FEV1%pred and ACT (P<0.05), however, the serum level of H2S were positively correlated with T-AOC, FEV1%pred and ACT (all P<0.05). ④ The serum levels of PC and MDA were affected by ROS (all P<0.05), especially MDA (β=0.411). Conclusion The oxidative stress is involved in the pathogenesis of bronchial asthma. ROS may cause damage to the body through NF-κB induced protein and lipid peroxidation. Endogenous H2S may play an antioxidant role by inhibiting ROS and NF-κB activity. ROS, PC and MDA could be used as monitoring indicators for bronchial asthma severity and control level. Endogenous H2S may be a potential target for the treatment of bronchial asthma. 
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