深低温停循环对大鼠额叶皮质Smad2和Smad4表达的影响

Effect of Deep Hypothermic Circulatory Arrest on Expression of Smad2 and Smad4 in Cortex Neuron of Rats

目的探讨深低温停循环对缺血缺氧大鼠额叶皮质信号转导分子2(Smad2)和信号转导分子4(Smad4)表达的影响.方法 40只SD大鼠经随机分组(其中4只为预灌注血液供体)后采用体外插管法建立大鼠闭胸式体外循环模型,三组动物分别经深低温停循环(DHCA,n=12,脑温<20℃,停循环10 min)、常温停循环(NTCA,n=12,脑温36.5℃～37.5℃,停循环10 min)和常温不停循环(NC,n=12,脑温36.5℃～37.5℃)处理后,快速断头取额叶皮质,液氮保存.免疫组化染色后图像分析系统处理判断Smad2和Smad4在缺血早期大鼠额叶皮质的表达情况.结果 Smad2和Smad4在DHCA组中较NTCA组和NC组表达均有明显升高,差异有统计学意义(P<0.05);Smad2和Smad4在NTCA组中较NC组表达有升高,差异有统计学意义(P<0.05).结论缺血缺氧可诱导大鼠额叶皮质Smad2和Smad4的表达,而深低温可以进一步促进额叶皮质内Smad2和Smad4的表达,反应性地增强脑损伤保护因子TGF-β1的作用,从而发挥脑保护作用.

Objective To investigate the effect of deep hypothermic circulatory arrest（DHCA） on expression of Smad2 and Smad4 in cortex neuron of rats.Method Forty SD rats were divided randomly into three groups： deep hypothermic circulatory arrest（DHCA） group（n =12）,normal temperature circulatory arrest（NTCA） group（n=12） and normal animal control（NC） group（n=12）,the next four rats were usedas the blood donor for other rats.The animal model of closed-chest DHCA was established in rats by means of external cannulation.In DHCA group,ten minute＇s circulatory arrest was performed after the temperature ofrectum less than or equal to 20 ℃（T 20 ℃） by external circulation and body surface cooling;in NTCA group,ten minute＇s circulatory arrest was performed in normal temperature by the same method;in NC group,tenminute＇s external circulation without circulatory arrest or deep hypothermia was performed.Cerebral cortexes were removed and dissociated after external circulation and then Smad2 and Smad4 were measured by immunohistochemisty,the results were analyzed by software SPSS11.0.Results The levels of Smad2 and Smad4 expression of DHCA group and NTCA group were much higher than NC group（P0.05）.The levels of Smad2 and Smad4 expression of DHCA group were much higher than NTCA group（P0.05）.Conclusions Ischemiacan induce the expression of Smad2 and Smad4 while deep hypothermia can upregulate Smad2 and Smad4 expression apparently.Deep hypothermia can protect brain against injury induced by ischemia and anoxia through enhancing the effect of the protective cytokine TGF-β1.