Abstract
A20 Aims: The aim of this study was to evaluate the role of the protein kinase B (PKB), phosphatidyl inositol-3 kinase (PI3-K) and BAD in normothermic ischemia-reperfusion (I-R) induced apoptosis in rat liver treated or not with Z-Asp-cmk caspase inhibitor. Methods: Rats were divided into two groups: group 1, control, PBS administration; group 2, Z-Asp-cmk treatment. Z-Asp-cmk was injected intravenously, 2 min prior to induction of 120 min of normothermic liver ischemia. PI3-K, PKB and BAD activities were measured in ischemic and non-ischemic lobes at different times after reperfusion. Immunohistochemical detection of apoptotic liver cells was carried out using the TUNEL method. Results: In control rats, PI3-K and PKB activities were inhibited in ischemic rat liver lobes. BAD phosphorylation was abolished after liver I-R. PKB activity was not modified by pre-treatment with Z-Asp-cmk caspase inhibitor whereas liver apoptosis was reduced. Conclusions: These results suggest that induction of apoptosis during I-R liver injury is triggered by the inactivation of the anti-apoptotic PI3-K/PKB pathway.
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