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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，作为信使参与全脑缺血再灌注大脑病理损伤的基因机制
OBJECTIVE: To investigate the expression of cfos gene in brain cells during global cerebral ischemia-reperfusion in rats and the effect of drugs on it. This study may provide a basis for exploring the gene mechanism of cerebral ischemia-reperfusion injury. METHODS: RNA was extracted from the brains of rats at different points during ischemia / reperfusion and electrophoresed with probe cfoscDNA. The images were analyzed to determine the relative levels of cfos mRNA in the brain. Results: The expression of cfos gene in brain increased from 20 minutes after ischemia to 20 minutes after reperfusion. The level of cfos gene expression in brain was significantly higher than that in control group (A value: 10.128 ± 1.454 vs 2.132 ± 0.623, P <0.01) (A value: 14.908 ± 1.862), then decreased and reperfusion for 90 minutes to reach and maintain normal levels, indicating that cfos gene early, fast, transiently high expression; with nimodipine Preconditioning of ischemic preconditioning significantly inhibited the expression of cfos gene in brain (A value: 2.312 ± 0.941) at 40 minutes after reperfusion for 30 minutes. CONCLUSION: The cfos gene is highly likely to mediate Ca2 + signaling as a messenger involved in the genetic mechanisms of brain injury following global cerebral ischemia-reperfusion