| Yan, Shi. F. reported in 《Nature Medicine》that Egr-1 activation played a central and unifying role in the pathogenesis of I/R tissue injury in 2000. When the mice were knocked out Egr-1 gene, the lung I/R injury of the Egr-1-null mice was alleviated and lung function was improved. The succedent researches indicated that inhibition of Egr-1 gene decreased the activation of inflammatory cell and improved organ function. Results of the former researches in our department showed that N-n-butyl haloperidol iodide (F2) inhibited Egr-1 expression of myocardium of rats and alleviated myocardial I /R injury. In order to confirm the role of Egr-1 in myocardial I/R injury, we applied Egr-1 AS-ODN to inhibit Egr-1 protein of myocardium in rat's myocardial I/R model. According to the results, we conclude that Egr-1 plays an important role in myocardial I/R injury.I. Methods1. Sprague-Dawley rat was administered 4 mg/kg of 5'-FITC-labelled AS-ODN for Egr-1 intravenously. After 24 h, the rat was executed and heart was taken out. Frozen sections were made and each slice was 5 urn in thickness. Then we observed the absorbtion of Egr-1 AS-ODN by fluorescence microscope and took pictures.2. Sprague-Dawley rats were randomly assigned to five groups: Sham group, I/R group, S group, Sc group and AS group. Each rat was administered intravenously 4 mg/kg of drug as described 24 h before ischemia. After 24 h, mycardial I/R model was produced by temporarily...
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