右丙亚胺预防脑缺血-再灌注蒙古沙鼠模型中神经细胞损伤及相关机制探讨  

Prevention of neuron injury by dexrazoxane in ischemia-reperfusion Mongolian gerbils models and investigation of related mechanisms

作　　者：杨立平[1] 

机构地区：[1]湖南省肿瘤医院药剂科,湖南长沙410013

出　　处：《中国现代医学杂志》2010年第8期1168-1170,1174,共4页China Journal of Modern Medicine

摘　　要：目的探讨脑缺血-再灌注(IR)蒙古沙鼠模型中脑神经元细胞的凋亡及相关自由基变化,并探讨这种变化与NF-γB和P38MAPK表达情况的关系。方法 60只雄性蒙古沙鼠(50～70 g)随机分为3组:假手术组、IR组和治疗组。其中,IR组应用动脉夹夹闭经总动脉5 min时间制作模型,而治疗组在IR之前通过腹膜注射的方法给予总剂量为150 mg的DEX,并观察各组NO、ROS、TBARS、亚硝酸盐/硝酸盐、细胞凋亡和NF-γB及P38MAPK蛋白表达情况。结果 IR可以明显改变鼠脑内的抗氧化/氧化环境,造成脑组织中NO降低,而ROS、TBARS及亚硝酸盐/硝酸盐均明显升高,同时提高了脑组织中NF-γB和P38MAPK的表达,降低了神经细胞的活力。相反,预先应用DEX处理过的蒙古沙鼠,则在上述指标发生与IR组相反的变化。结论 DEX可以明显改善鼠脑内的抗氧化/氧化环境,使IR沙鼠脑内回复抗氧化/氧化平衡,提高细胞生存率,而这种变化可能与NF-γB和P38MAPK表达降低相关。【Objective】To investigate the neuron apoptosis and related free radicals in the ischemia-reperfusion（IR） Mongolian gerbils models,observe the relationship between such changes and the expression of NF-γB and P38MAPK protein as well as.【Methods】 Sixty male Mongolian gerbils were divided into three groups randomly： sham-operation group,IR group and treatment group.IR model was made by using the artery clips to occlude the carotid artery for 5 min,in treatment group,a total of 150mg DEX was administrated in to each gerbil by peritoneal injection.NO,ROS,TBARS,nitrite/nitrate,apoptosis and expression of both NF-γB and P38MAPK proteins were observed.【Results】 IR could alter the antioxidant/oxidant environment and decrease NO and survival of neurons in brain tissue.In IR models,ROS,TBARS,nitrite/nitrate and NF-γB and P38MAPK protein expression increased.However,the above-mentioned index in the treatment group changed adversely.【Conclusion】 DEX can ameliorate the antioxidant/oxidant environment into the balance state,increase the anti-distress capacity to IR,such changes may be related to the decreased expression of NF-γB and P38MAPK proteins.

关 键 词：缺血-再灌注 右丙亚胺 P38MAPK NF-γB 抗氧化/氧化 

分 类 号：R654.1[医药卫生—外科学] R-332[医药卫生—临床医学]