ABSTRACT
BACKGROUND: Disoprofol has anti-apoptosis impact so that it can protect the neurons from damage caused by ischemia. However, it needs further study on the mechanism of anti-apoptosis of it. OBJECTIVE: To investigate the effects of disoprofol to cell apoptosis and expression of apoptosis-associated gene in rats during reperfusion after global ischemia.DESIGN: A randomized controlled trial.SETTING: Department of Neurosurgery of Beijing Tiantan Hospital.MATERIALS: The experiment was conducted in Beijing Neurological Surgery Research Institute of Capital University of Medical Sciences during January 2003 to January 2004. A total of 23 adult male Wistar rats were randomly divided into ischemic group( n =9), disoprofol group( n =9) and sham operation group( n = 5).INTERVENTIONS: To prepare global ischemia-reperfusion model of rats. Disoprofol was injected into vein with dose of 1.5 mL/hour after reperfusion started in disoprofol group and lasted for 30 minutes. Five rats were selected from each group to be removed brain after reperfusion for 24 hours. Apoptosis rate and necrosis rate were detected by flow cytometer. Four rats selected from ischemic and disoprofol group were detected differential expression of apoptosis associated genes by gene chip combining image analysis techniques.MAIN OUTCOME MEASURES: ① apoptosis rate and necrosis rate; ②expression of apoptosis-associated gene detected by gene chip.RESULTS: The apoptosis rate[(7.01 ±0.79)% ] and necrosis rate[ ( 12. 80 ± 0. 92) % ] of neurons of hippocampus in disoprofol group were much lower than those of ischemic group [ (10. 89 ± 0. 80)%, (16. 67 ± 1.04)% ](P ＜ 0.01) . Compared with ischemic group, the three apoptosis associated genes including apoptotic prote ase activating factor 1 (APAF1), death effector domain containing testicular molecular mRNA(DEFT) and STM-2 were down regulated.CONCLUSION: Disoprofol can protect the brain and its mechanism might be related to the down regulation of three apoptosis associated genes including APAF1, DEFT and STM-2.