氯喹、SOD 防治脑缺血再灌注损伤的实验研究  

Chloroquine or SOD protecting rat , s brain from postischemic reperfusion injury

作　　者：夏绪刚[1,2] 黄兆民[1,2] 欧阳珊 

机构地区：[1]湛江广东医学院附属医院神经内科 [2]湖南医科大学

出　　处：《中风与神经疾病杂志》1997年第2期84-86,共3页Journal of Apoplexy and Nervous Diseases

摘　　要：探讨氯喹、超氧化物歧化酶（ＳＯＤ）防治脑缺血再灌注损伤的效果。用４血管阻断法造成大鼠全脑缺血，３０ｍｉｎ后再恢复双侧颈总动脉血流３０ｍｉｎ，此时大鼠脑组织磷脂酶Ａ（ＰＬＡ）活性和内皮素（ＥＴ）、过氧化脂质（ＬＰＯ）含量显著增高，而ＳＯＤ活性和维生素Ｅ（ＶｉｔＥ）含量明显降低，大脑皮层神经细胞和血脑屏障明显损害。预防用氯喹或ＳＯＤ治疗，部分抑制了ＬＰＯ、ＥＴ含量的增高和ＳＯＤ活性下降，明显减轻脑神经细胞和血脑屏障损伤程度；但对ＶｉｔＥ含量都无明显影响。氯喹、ＳＯＤ对缺血再灌注脑损伤有一定的防治作用。Protective effects of chloroquine or superoxide dismatase(SOD) on brain of Wistar rats with cerebral postischemic reperfusion was studied. The complete cerebral ischemic models were made by 4 vessel occlusion in awake Wistar rats. By 30 min reperfusion after 30 min complete cerebral ischemia in rats, phospholipase A 2 (PLA 2 ) activities and values of endothelins(ET) and lipid peroxidation(LPO) increased(all P<0.05), but SOD activities and vitamin E(Vit E) Valaues decreased(all P<0.05) in brain tissues. At the same time, Blood brain barriers and cortex neuronal ultrastructures were damaged severely. By pretreatment with chloroquine or SOD, the increases of PLA 2 activities and levels of ET and LPO, the decreases of SOD activities in brain tissue were all inhibited significantly(all P<0.05). At the same time, the cerebral postischemic reperfusion injury was reduced. There were no significant effects on values of Vit E in brain tissue. Effects of chloroquine can partly inhibit PLA 2 activities in brain tissue. Chloroquine and SOD have protective effects on brain in Wistar rat with cerebral postischemic reperfusion.

关 键 词：脑缺血 再灌注损伤 氯喹 超氧化物歧化酶 防治 

分 类 号：R743.05[医药卫生—神经病学与精神病学]