摘要
目的:探讨酸性神经肽1(BANP-1)对血管性痴呆(VD)小白鼠脑内超氧化物歧化酶(SOD)、丙二醛(MDA)和一氧化氮(NO)的影响。方法:将小白鼠随机分为5组,每组12只,除正常对照组外,其余4组分别在高脂血症的基础上,用颈总动脉缺血再灌注法建立VD模型,其中1组为VD模型组,其它3组在手术后分别给予BANP-11.5g/(kg·d)、0.75g/(kg·d)、0.3g/(kg·d),连续灌胃15d,每天1次,每次1ml。15d后将小白鼠断头处死并立即在冰盘中开颅取脑做组织匀浆,取上清液测MDA、NO含量和SOD活性。结果:VD模型组较正常对照组脑内SOD活性明显降低(P<0.01),MDA、NO含量明显升高(P<0.01)。BANP-1各治疗组较VD模型组脑内SOD活性明显升高(P<0.01),MDA、NO含量明显下降(P<0.01)。结论:BANP-1可明显升高VD小白鼠脑内SOD活性,降低MDA和NO含量。
Objective:To probe the changes of SOD,MDA and NO in the brains of VD mice by bovine acidic neuropeptide-1(BANP-1).Methods:Mice were divided into five groups(12in each group).Mice in four groups were made hyperlipid and underwent common carotid artery is chemia and reperfusion.After the operation,BANP-11.5g /kg·d,0.75g /kg·d and0.3g /kg·d was administered orally respectively to the mice in groupsⅢ,ⅣandⅤ.The process lasted for15days,once every day,1ml each time.Then all the mice were decapi tated and the brain was homogenized and centrifu galized for the measurement of SOD,MDA and NO.Results:Compared with that in the normal control group,the activity of SOD in mice of VD model group mice decreased sig nificantly(P<0.01),but the content of MDA and NO increased sig-nificantly(P<0.01).Compared with that in the VD model group,SOD in the groups given BANP-1increased significantly(P<0.01),while MDA and NO decreased significantly(P<0.01).Conclusion:BANP-1can sig nifi-cantly in crease the activity of SOD and decrease the con tent of MDA and NO in brains of VD mice.
出处
《山东大学学报(医学版)》
CAS
2003年第1期14-15,18,共3页
Journal of Shandong University:Health Sciences
关键词
血管性痴呆
酸性神经肽1
超氧化物歧化酶
丙二醛
一氧化氮
Dementia,vascular
Bovine acidic neuropeptide-1
Superoxide dismutase
Malondi alde-hyde
Ni tric oxide