Effects of alcohol on hippocampal apoptosis-inducing factor and caspase-3 expression in cerebral ischenda/reperfusion in rats

Abstract

Objective To investigate the effects of alcohol on hippocampal apoptosis-inducing factor （AIF） and caspase-3 expression in cerebral ischemia/reperfusion in rats.Methods Sixty-eight healthy adult male Wistar rats were randomly divided into a sham operation goup （n =4） and a saline control group as well as low-dose （1.0 g/kg）, medium-dose （1.5 g/kg） and high-dose （2. 0 g/kg） ethanol groups. The saline control group and each dose alcohol group were redivided into ischemia/reperfusion 0, 1,2 and 3 h subgroups according to the intervention time points （n =4 in each group）. A model of middle cerebral artery ischemia/reperfusion in rats was induced by the suture method. The corresponding doses of ethanol or an equal volume of saline were injected intraperitoneally at ischemia for 2 h and reperfusion for 0, 1, 2 and 3 h in the alcohol groups and the saline control group. At ischemia for 2 hand reperfusion for 24 h, the neurological deficit in rats was evaluated by using behavioral score. Immunohistochemistry assay was used to detect the expressions of AIF and caspase- 3 in the hippocampus of ischemic sides at ischemia for 2 hand reperfusion for 24 h. Results The behavior evaluation showed that the neurological deficit score was 0 in the sham operation group. The neurological deficit scores in the different dose ethanol groups were sigaificantly lower than those in the saline control group at the same intervention time points （all P= 0. 000）, and there were significant differences between the same intervention time points in the different dose ethanol groups （all P =0. 000）. The high-dose ethanol group was the lowest. There were no sigfificant differences between the different intervention time points in the same dose ethanol groups （all P 〉 0. 05）. Immunohistochemistry revealed that the numbers of positive ceils of MF and caspase-3 in the sham operation group were 17. 21 ± 2. 86 and 20. 60 ± 4. 39, respectively, and they were significantly less than those in the saline control group and the each dose ethanol group at ischemia/reperfusion 0 h （all P =0. 000）; the number of positive cells of hippocampal AIF and caspase-3 in the different dose ethanol groups were all signicantly less than those in the saline control goup at the same intervention time points （all P =0. 000）. There were signifieant differences between the same intervention time points in the different dose ethanol groups （all P = 0. 000）, and the high-does ethanol group was the lowest. There were no sigaificant differences between the different intervention time points in the same dose ethanol groups （all P = 0. 000）. Conclusion Alcohol has protective effect on the cerebral tissue in ischemia/reperfusion injury in rats. Its mechanism may be associated with the inhibition of AIF and caspase-3 expression. Key words: Brain Ischerrha; Ethanol; Apoptosis Inducing Factor; Caspase 3; Hippocampus; Neuroprotective Agents; Disease Models, Animal; Rats