氯酯醒对小鼠缺血再灌注脑损伤的保护作用研究  

CENTROPHENOXINE IMPROVES ISCHEMIA AND REPERFUSION-INDUCED NEURONAL DEGENERATION IN MICE

作　　者：廖赟[1] 李玲[1] 刘学源[2] 

机构地区：[1]上海市第十人民医院药剂科,上海200072 [2]上海市第十人民医院神经内科,上海200072

出　　处：《广西医科大学学报》2006年第5期714-716,共3页Journal of Guangxi Medical University

基　　金：上海市自然科学基金重点资助项目(No.044119634)

摘　　要：目的:采用小鼠双侧颈总动脉缺血再灌注模型,观察氯酯醒对缺血再灌注脑损伤的改善作用。方法:重复缺血10 min于再灌后2、244、8 h分别取脑组织,密度梯度法检测脑组织含水量的变化,生化测量突触膜Na+-K+-ATP酶、Ca2+-ATP酶活性。HE染色观察组织形态学改变。结果:急性缺血再灌注能引起小鼠脑组织水肿,伴随着Na+-K+-ATP酶和Ca2+-ATP酶活性降低,以及皮层海马神经元损害。术前3 d预服氯酯醒(100 mg/kg,1次/d),可显著减轻脑组织水肿,提升异常降低的ATP酶活力,改善神经元结构异常。结论:氯酯醒的神经元保护作用可能与抑制脑水肿的发生,改善脑缺血后能量代谢失衡和钙离子超载等作用有关。Objective：To study the effects of centrophenoxine （CPH, Meclofenoxate） on ischemia / reperfusion （I/R） -induced deficits in mice. Methods：I/R in mice was performed and cerebellar water content was measured by density gradient method. Spectrophotometrical techniques were used to assay Na^＋-K^＋-ATPase and Ca^2＋-ATPase activities. Morphological change was examined by HE staining. Result： All mice were subjected to cerebral I/R-triggered changes in morphology and biochemistry including reductions of Na^＋- K^＋-ATPase and Ca^2＋-ATPase activities, along with the increases in brain water content. Oral administration of CPH（100 mg/kg, once per day） markedly reduced morphologic damage, alleviated disturbance of energy metabolism and attenuate brain edema. Conclusion：The present finding implicated that the neuro-proective effects of CPH may proceed through restrain brain edema,amelioration the disbanlance of energy metabolism and Ca^2＋ overload pathway.

关 键 词：氯酯醒 缺血性脑损伤 脑水肿 NA^+-K^+-ATP酶 CA^2+-ATP酶 小鼠 

分 类 号：R965[医药卫生—药理学]