实验性吸烟大鼠氧化抗氧化指标的研究

目的探讨吸烟在慢性阻塞性肺疾病(COPD)氧化/抗氧化失衡发病机制中的作用,为进一步开发COPD的抗氧化药物治疗提供理论依据。方法Wistar大鼠32只,随机分为不吸烟组和吸烟1个月组、2个月组、3个月组,每组8只。采用化学发光法检测各组血清、支气管肺泡灌洗液(BALF)中超氧化物歧化酶(SOD)、还原性谷胱甘肽(GSH)、脂质过氧化物(MDA)含量。结果①吸烟1个月、3个月组血清GSH(327±199)μmol/L,(392±136)μmol/L均较不吸烟组(294±156)μmol/L增高,但差异无统计学意义;吸烟3个月组血清GSH(392±136)μmol/L较2个月组(174±7)μmol/L增高,差异有统计学意义(P<0.05);各组BALF中GSH含量的变化差异无统计学意义。②吸烟2个月组血清SOD活力(116±36)kU/L较不吸烟组(104±13)kU/L、吸烟1个月组(100±13)kU/L、吸烟3个月组(100±12)kU/L均增高,差异有统计学意义(P<0.05);各组BALF中SOD活力的变化差异无统计学意义。③吸烟各组血清及BALF中MDA含量均较不吸烟组增高,但差异无统计学意义(P>0.05)。结论不同吸烟时间引起机体氧化抗氧化指标的变化不同。抗氧化能力减弱所致氧化/抗氧化失衡是吸烟导致COPD的重要发病机制。

The study of oxidantion/antioxidantion in somking experimental rats

Objective To investigate the change of SOD,MDA,GSH in serum of smoking rats,as well as the variations of them in BALF.It can be used to provide the objective evidence in studying the pathogenesis of COPD.Methods Wistar rats (n=32) were randomized devided into without smoking group and smoking 1 month group, 2 month group and 3 month group, 8 in each group. The serum and BALF of each group were collected,and the level of SOD,MDA,GSH in serum and BALF was detected.Results ①The serum GSH content in smoking 1 month group (116±36)μmol/L, smoking 3 month group (392±136)μmol/Lwerehigherthanthatofwithout smoking group (294±156)μmol/L;3 month group (392±136)μmol/L was significantly higher in the serum GSH content than of 2 month group (175±70)μmol/L,(P<0.05).②The serum SOD activity (116±36)kU/L in smoking 2 month group was significantly higher thanthoseofwithoutsmoking group (104±13)kU/L,smoking 1 month group (100±13)kU/L and smoking 3 month group (100±12)kU/L (P<0.05 respectively).③The MDA content in serum and BALF in all smoking groups was higher than that of without smoking group,but no statistic significance was found (P>0.05 respectively).Conclusion Different smoking time can result in the change of the level of SOD,MDA,GSH in serum and BALF of the smoking rats.The increase of oxidant,decrease of antioxidant and imbalance of oxidantion/antioxidantion might play an important role in COPD induced by smoking.