氯胺酮对沙土鼠脑缺血再灌注损伤后细胞凋亡的影响  

Effect of Ketamine on Neurons Apoptosis after Cerebral Ischemia-Reperfusion in Gerbils

作　　者：周益锋[1] 邬伟东[1] 柳子明[1] 周海燕[1] 陈钢[1] 王慧华[1] 

机构地区：[1]浙江大学医学院附属第二医院麻醉科,310009

出　　处：《天津医药》2003年第5期302-303,共2页Tianjin Medical Journal

摘　　要：目的 :研究氯胺酮对沙土鼠脑缺血再灌注损伤后细胞凋亡状态及相关基因bax、bcl 2表达的影响。方法 :沙土鼠全脑缺血模型 ,缺血10min ,再灌注24h。分为假手术组、缺血再灌注组和氯胺酮组。采用TUNEL法原位标记DNA片段检测凋亡细胞 ,采用SP法进行bax、bcl 2的免疫组织化学染色。结果 :缺血再灌注组及氯胺酮组脑组织中TUNEL及bax阳性细胞数明显多于假手术组(P<0 .01) ;氯胺酮组阳性细胞数目明显低于缺血再灌注组(P<0 .01)。bcl 2阳性细胞数3组间比较无明显差异。结论 :氯胺酮减少沙土鼠脑缺血再灌注损伤后细胞的凋亡 ,bax/bclObjective:To investigate the effect of ketamine on neurons apoptosis after cerebral ischemiˉaˉreperfusion in gerbils.Methods:Thirty gerbils were randomly assigned to3groups:shamˉoperative(SO)group,ischemiaˉreperfusion(IR)group and ketamine treatment(K)group.Apoptosis was detected by termiˉnalˉdeoxynucleotidyl transfarase mediated nick end labeling(TUNEL),and bax,bclˉ2were detected by imˉmunohistochemistry.Results:Compared with SO group,there were more TUNEL and bax positive cells in IR and K groups(P<0.01).There was no obvious difference of the numbers of bclˉ2positive cells among the3groups(P>0.05).Conclusion:Ketamine can reduce the neurons apoptosis and bax/bclˉ2value after cerebral ischemiaˉreperfusion in gerbils.This effect of it might be an important mechanism which protects the cerebrum from ischemiaˉreperfusion damage.

关 键 词：沙土鼠 脑缺血 再灌注损伤 细胞凋亡 BAX基因 BCL-2基因 

分 类 号：R743.31[医药卫生—神经病学与精神病学] R972[医药卫生—临床医学]