Abstract:

This study was to observe the effect of hyperbaric oxygen (HBO) on the expressio ns of caspase-3 in hippocampus following transient forebrain ischemia, and to find out the possible mechanism of HBO treatment. C57BL/6N mice were divided into three groups: sham-operated group (control), ischemia/reperfusion(I/R) group and HBO treatmen t after I/R group. Transient forebrain ischemia was induced by bilateral common carotid artery occlusion for 20 min. Hippocampus was obtained at reperfusion ti me poin ts of 6 h, 12 h, 24 h and 48 h respectively after 20 min of ischemia. RT-PCR wa s used to detect the expression of caspase-3 mRNA, and Western Blotting was use d to detect the level of caspase-3 protein. Experimental data showed that caspase-3 mRNA and procaspase-3 level increased in hippocampus in I/R groups and HBO groups. The difference was significant(P< 0.05) when compared with express ion levels in sham-operated mice. There was no significant alteration in expres s ion levels between every I/R group and HBO treatment group of corresponding time point(P> 0.05). These data indicate that ischemia/reperfusion which induces caspase-3 mRNA expression and increases transcription of caspase-3 is the mean reason fo r procaspase-3 increase. Caspase-3-dependent apoptosis is involved in ischemia /re perfusion injury. The HBO treatment project has no significant effect on caspase-3 mRNA and procaspase-3.

Key words: cerebral ischemia/reperfusion, hype rbaric oxygen, caspase-3, expression