【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/bcl 2比值较再灌注组相对降低可能为此作用的机理之一更多还原

【Abstract】 Objective: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.更多还原