全脑缺血再灌注大鼠大脑c-fos基因表达的实验研究

Experimental study on gene expression of cfos in cerebrum after complete global brain ischemiareperfusion in rats

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 32Plabeled 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:10128±1454 vs.2132±0623,P<001),and it reached peak levels at 40 minutes of reperfusion (A:14908±1862).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:2312±0941).Conclusions:These results indicate that cfos gene probably involves in the molecular mechanism of cerebrum damage during complete global brain ischemiareperfusion.