心肌肽素预先给药对大鼠海马神经元缺氧复氧损伤的影响  

Effects of cardiomyopeptidin pretreatment on anoxia-reoxygenation injury to hippocampal neurons in rats

作　　者：刘荣国[1] 汪炜健[1] 何爱霞[1] 李立环[1] 

机构地区：[1]中国医学科学院中国协和医科大学阜外心血管病医院麻醉科,北京市100037

出　　处：《中华麻醉学杂志》2005年第10期759-761,共3页Chinese Journal of Anesthesiology

摘　　要：目的 研究心肌肽素(CMP)预先给药对原代培养大鼠海马神经元缺氧复氧损伤的影响 及相关机制。方法原代培养SD大鼠海马神经元,随机分为4组:对照组、缺氧复氧组、CMP 10 μg／ml 组、CMP 100 μg／ml组。对照组不实行任何处理,缺氧复氧组海马神经缺氧4 h复氧48 h,建立神经元缺 氧复氧损伤模型。CMP 10 μg／ml、CMP 100 μg／ml组缺氧前30 min于培养液中加入相应浓度的CMP,缺 氧复氧组加入相应的溶剂。采用四唑蓝比色法测定神经元的细胞活力,采用细胞免疫化学法测定神 经元Bcl-2蛋白表达水平。结果与对照组比较。缺氧复氧组、CMP10 μg／ml组、CMP100μg／ml组海马 神经元缺氧复氧后细胞活力降低,Bcl-2蛋白表达升高(P<0．05),CMP 100 μg／ml组细胞活力及Bcl-2 蛋白表达高于缺氧复氧组和CMP10μg／ml组(P<0．05),CMP 10μg/ml组与缺氧复氧组之间上述两指 标比较差异无统计学意义(P>0．05)。结论CMP100μg／ml可增强Bcl-2蛋白的表达,减轻缺氧复氧 后海马神经元损伤。Objective To investigate the protective effects of cardiomyopeptidin （CMP） pretreatment against hippocampal neuronal injury caused by anoxia-reoxygenation and the underlying mechanism. Methods Hippocampal neurons were isolated from neonatal SD rats and cultured for 9-10 days. The cultured primary hippocampal neurons were randomly divided into 4 groups： （ Ⅰ ） control group; （ Ⅱ ） anoxia-reoxygenation group （A-R）; （Ⅲ） CMP 10 μg·ml^-1 group （CMP1） and （Ⅳ） CMP 100 μg·ml^-1 group （CMP2）. In A-R group hippocampal neurons were subjected to 4 h anoxia （ cultured in 95 % N2 ＋ 5 % CO2 ） and 48 h reoxygenation （cultured in aerobic environment）. In group Ⅲ and Ⅳ CMP was added to culture media with end-concentration of CMP 10 μg·ml^-1 or 100 μg·ml^-1 before oxygen-deprivation. Neuronal viability was assessed by MTT method and Bcl-2 protein expression was determined by immuno-cytochemistry. Results The optical density （OD） value of hippocampal neurons and the Bcl-2 expression were significantly higher in group Ⅳ （CMP2） than those in group Ⅱ （A-R） and Ⅲ （CMP1） （P 〈 0.05）. However there was no significant difference in OD value and Bcl-2 expression between group Ⅱ and Ⅲ Conclusion CMP 100 μg·ml^-1 has protective effect on hippocampal neurons against anoxia-reoxygenation injury through upregulation of Bcl-2 expression in the neurons.

关 键 词：肽类 细胞低氧 神经元 海马 

分 类 号：R96[医药卫生—药理学]