摘要
目的 探讨脑组织二硫键异构酶 (PDI)的变化在脑缺血—再灌注损伤 (CIRI)中的意义。方法 制作Wistar大鼠动物模型 ,随机分为假手术对照组、缺血—再灌流组和重组人硫氧还蛋白酶 (还原型rhTRX )治疗组。动态观察正常对照、实验对照和rhTRX治疗组血浆及脑组织一氧化氮 (NO)水平、超氧化歧化酶 (SOD)活性、脑组织二硫键异构酶 (PDI)的变化。结果 脑缺血 再灌溉损伤时 ,血浆和脑组织NO水平、超氧化歧化酶 (SOD)活性与缺血前比较明显下降 (P <0 0 5 )。在rhTRX组 ,NO及SOD的代谢物明显增多 (P <0 0 1) ,rhTRX组与对照组相比较 ,PDI还原硫基 (free thiols)的细胞水平明显增加。结论 再灌注损伤中氧自由基与NO结合 ,使NO的减少 ,是脑损害的直接原因。而PDI通过降低氧自由基而达到保护和恢复NO的功能 。
Objective To investigate the changes and significance of protein disulfide isomerase in rats with ischemic brain damage.Methods Using an animal model of 39 rats which were randomly divided into false CIRI group;CIRI group and CIRI with rhTRX groups.Altered amount of several cellular metabolites in plasma and brain during CIRI were measured, including nitric oxide(NO), and superoxidedismutase(SOD).The level of reduced form of protein disulfide isomerase(PDI) in brain tissue was analysed by MPB labelling and western blotting.Results Level of NO and SOD in plasma and cerebral tissue was decreased in CIRI group( P <0 05).In the rhTRX group, however, the level of both metabolites was restored significantly( P <0 01).Cellular level of reduced PDI was higher in CIRI rhTRX groups than that of the group with CIRI alone.Conclusion Reactive free oxygen during reperfusion could be a direct reason for brain damage, while PDI led to reduction of reactive oxygen level, so that recovery of NO and prevented cerebral tissue from the oxidation pressure.
出处
《重庆医学》
CAS
CSCD
2002年第8期713-715,共3页
Chongqing medicine
