硫酸锌对大鼠急性脑缺血再灌注损伤的保护作用  

Protection of zinc sulfate on acute cerebral ischemia reperfution injury in rats

作　　者：段文贞[1,2] 梁月琴[1,2] 汤允昭[1,2] 

机构地区：[1]山西医学院药理学教研室 [2]中国医学科学院中国协和医科大学药物研究所药理室

出　　处：《中国药理学通报》1997年第1期39-42,共4页Chinese Pharmacological Bulletin

摘　　要：目的：观察硫酸锌对脑缺血再灌注损伤的作用。方法：用Ｐｕｌｓｉｎｅｌｉ四动脉结扎法造成大鼠急性前脑缺血４０ｍｉｎ后再灌注１ｈ的损伤模型，同时应用Ｆｕｒａ－２／ＡＭ荧光指示剂测定硫酸锌对胎鼠脑细胞内游离钙浓度的影响。结果：静脉注射硫酸锌１０ｍｇ·ｋｇ－１可降低钙在脑细胞内累积及丙二醛含量升高；减轻脑水肿并缓解脑损伤引起的ＬＤＨ释放；改善ＥＥＧ的抑制状态。在胎鼠脑细胞悬液中，硫酸锌（１００～３００μｍｏｌ·Ｌ－１）可抑制高钾和Ｌ－谷氨酸引起的细胞内钙升高。结论：硫酸锌对急性再灌注脑损伤有保护作用，此作用与其防止钙超载、抗脂质过氧化物产生有关。AIM: Cerebral protection of zinc sulfate was observed on the acute cerebral ischemia reperfusion injury in rats. METHODS: Animal model was produced by occlusion of four vessels. At the same time, free intracellular calcium concentration was measured by using calcium sensitive fluorescent indicator Fura 2/AM in isolated embryonic rat brain cells. RESULTS: Pretreatment with zinc sulfate (10 mg·kg -1 , iv) significanty declined calcium accumulation and malondialdehyde content; inhibited brain edema and lactic dehydrogenase releasing from brain tissue; promoted the recovery of EEG activities. ZnSO 4 (100～300 μmol·L -1 ) inhibited the Ca 2+ i elevation induced by high extracellular potassium (50 mmol·L -1 ), with an IC 50 value of 190(95% confidence limits: 150￣230) μmol·L -1 , and blocked the L glutamate (100 μmol·L -1 ) stimulated increase of Ca 2+ i with an IC 50 of 210 (95% confidencelimits: 170￣250) μmol·L -1 . CONCLUSION: Zinc sullfate protected brain tissue from ischemia reperfusion injury through reducing calcium accumulation and anti lipid peroxidation.

关 键 词：硫酸锌 保护作用 再灌注损伤 过氧化脂质 脑缺血 

分 类 号：R977.5[医药卫生—药品]