摘要
目的:研究大鼠全脑缺血再灌注时大脑细胞cfos基因表达及药物对其的影响,为探讨脑缺血再灌注损伤的基因机制提供依据。方法:从不同缺血再灌注时点大鼠的大脑提取RNA,与探针cfoscDNA进行打点分子杂交,图像经分析测出各时点大脑cfos基因mRNA的相对水平。结果:大脑cfos基因表达从缺血20分钟开始,再灌注20分钟表达水平显著高于对照组(A值:10.128±1.454比2.132±0.623,P<0.01),再灌注40分钟达高峰(A值:14.908±1.862),随后下降,再灌注90分钟达到并维持正常水平,显示cfos基因早期、快速、一过性高表达;用尼莫地平缺血前预处理能显著抑制缺血30分钟再灌注40分钟时大脑cfos基因表达(A值:2.312±0.941)。结论:cfos基因极可能介导了Ca2+的信息。
Objective:To investigate the gene expression of cfos in cerebrum at various time points after brain ischemiareperfusion and effect of nimodipine on the expression,providing evidence to elucidate the molecular mechanism of brain injury.Methods:The cerebrum was obtained in rats after complete global brain ischemiareperfusion.Total cellular RNAs were isolated by acid guanidine isothiocyanated extraction,and the RNAs were hybridized to 32Plabeled cDNA and analyzed by automatic system.Results:Expression of cfos gene in cerebrum was rapidly induced by 20minute ischemia,it increased obviously at 20 minutes of reperfusion (A:10128±1454 vs.2132±0623,P<001),and it reached peak levels at 40 minutes of reperfusion (A:14908±1862).It started to decline markedly as early as 60 minutes of reperfusion,and it returned to the normal value recovered at 90 minutes of reperfusion.However,pretreatment with nimodipine prevented the gene expression of cfos at 40 minutes of reperfusion (A:2312±0941).Conclusions:These results indicate that cfos gene probably involves in the molecular mechanism of cerebrum damage during complete global brain ischemiareperfusion.
出处
《中国危重病急救医学》
CAS
CSCD
1998年第4期210-212,共3页
Chinese Critical Care Medicine
关键词
脑缺血
再灌注损伤
C-FOS基因
分子杂交
ischemiareperfusion injury\ \ cfos gene\ \ hybridization\ \ nimodipine