摘要
目的研究丁基苯酞对短暂性局部脑缺血大鼠脑线粒体ATPase,抗氧化酶活性和脂质过氧化的影响。方法采用短暂性大脑中动脉阻断术(tMCAO)模型,应用生物化学方法,测定神经细胞线粒体ATPase活性,超氧化物歧化酶(superoxide dismutase,SOD),谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px),过氧化氢酶(catalase,CAT)的活性和MDA的含量。结果(1)大鼠tMCAO后线粒体ATPase活性均有不同程度的下降,于tMCAO前10min腹腔注射丁基苯酞(NBP)(5~20mg /kg)能明显升高线粒体Na+K+-ATPase和Ca 2+ -ATPase活性。(2)在缺血溶剂组,SOD活性和线粒体GSH-Px活性显著下降,而MDA的含量则明显升高。于缺血前10min,腹腔注射NBP(20mg /kg)能明显增加缺血侧神经细胞线粒体和脑皮层总SOD的活性,然而对CuZn-SOD活性无明显作用。腹腔注射20mg /kg NBP能显著升高线粒体GSH-Px的活性,而腹腔注射10、20mg /kg NBP能明显降低缺血脑线粒体MDA的含量(P<0.05=。(?
Objective The aim of the present study was designed to explore the effect of(±)-3-n-butylph-thalide(NBP)on ATPase,anti-oxidant enzymes activities and lipid peroxidation of mitochondria and cerebral cortex in rats subjected to24hours of reperfusion following2hours of cerebral ischemia(tMCAO).Methods Activities of SOD(Superoxide Dismutase),GSH-Px(glutathione Peroxidase,)and CAT(Catalase),and MDA level of mitochondria or cortex were measured by using biochemical met-hods in tMCAO rats.Results(1)The activities of mitochondrial Na + K + -ATPase,Ca 2+ -ATPase and Mg 2+ ATPase were found to decrese significantly in the vehicle group(ishemia+saline).Pre-treatment with NBP(5,10,20mg /kg,ip)10min before tMCAO markedly enhanced the activities of Na + K+-ATPase and Ca 2+ -ATPase,compared with vehicle group.(2)The activities of SOD and mitochondrial GSH-Px were decreased and MDA level increased in vehicle groups as compared with that in sham group(non is chemia+saline).NBP(20mg /kg,ip)significantly enhanced total mitochondrial SOD activity,and also enhanced cerebral cortex total SOD activity(in5,10,20mg /kg groups).However,it had no obvious effect on CuZn-SOD activity.NBP(20mg /kg ip)markedly increased mitochondrial(but not in cerebral cortex)GSH-Px activity;NBP10,20mg /kg markedly decreased mitochondrial MDA level compared with that in vehicle group (P<0.05=.(3)The action of raceme NBP on the increase of the activities of ATPase and antioxidative enzymes seemd to be beneficial than that of(-)-NBP or(+)NBP.Conclusion The results suggest that NBP improves energy pump and subsides oxidative injury which may contribute to its anti-neuronal apoptotic effect.
出处
《中国医学科学院学报》
CAS
CSCD
北大核心
2002年第1期93-97,共5页
Acta Academiae Medicinae Sinicae
基金
国家科委1035工程重大项目基金(94-ZD-01)
国家自然科学基金重大项目基金(29790122)~~