Ischemic postconditioning used at the right time after initial ischemia is able to protect the most vulnerable CA1 hippocampal neurons. Alteration of ubiquitin immunoreactivity (UIR) was studied after 7 days of reperfusion in 4 experimental groups of rats (1) 10 min of ischemia, (2) 10 min of ischemia followed by ischemic postconditioning (5 min of ischemia done after 2 days of reperfusion). Extract of Ginkgo biloba (EGb 761, 40 mg/kg; p.o.) was administered 5 h after 10 min of ischemia both in ischemic group (3) or ischemia/postconditioning group (4). Quantitative analysis showed signifi cant decrease (45.0 ± 9.7) of ubiquitin positive CA1 neurons in group (1) in comparison to sham control (187.5 ± 15.1) and nonsignifi cant increase of neuronal UIR (74.8 ± 22.4) in group (3) with EGb 761 administration. Ischemia/postconditioning (2) showed neuroprotection and signifi cant increase of ubiquitin positive CA1 neurons (133.4 ± 14.3). Ischemia/ postconditionig combined with antioxidant EGb 761 (4) revealed suppression of neuroprotective effect of delayed ischemic postconditioning. Moreover, signifi cant decrease of ubiquitin positive neurons (10.8 ± 2.4) in CA1 region was observed. Our results suggest that delayed ischemic postconditioning is able to prevent ischemia induced neurodegeneration while antioxidant used after initial ischemia followed by postconditioning fully abolishes this effect. This study was supported by VEGA grants: 1/4237/07, 2/0141/09 and APVV LPP 0235-06.
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