RESUMO
OBJECTIVE: The warm ischemia-reperfusion injury confines the prevalence of allografts. To improve the success rate of allotransplantation, we designed experiments to study the mechanism of calcium-calmodulin-dependent protein kinase type 2 (CaMK II) in ischemia-reperfusion (I/R) injury. MATERIALS AND METHODS: We established the I/R model in SD rats and performed the liver transplantation (LT). As a result, the expression of CaMK II in tissues was detected. CaMK II was interfered with and overexpressed by the transference of the lentivirus vector, and the hepatocyte apoptosis and viability were inspected. At the same time, the content of cytochrome c and apoptosis-inducing factor (AIF) were determined. The measurement of mitochondrial membrane potential and detection of intercellular calcium levels were performed. RESULTS: The expression of CaMK II significantly increased and is highly corresponded with the duration of warm ischemia. In BRL-3A cells and liver tissues, increased cellular apoptosis and less viability had been observed in the CaMK II overexpression group. Cytochrome c and AIF were also largely increased compared to the interfered group. Moreover, apparent mitochondrial membrane potential loss has also been detected in the CaMK II overexpression group. CONCLUSIONS: It suggested that CaMK II induces cell apoptosis. Our findings may give a novel indication that inhibition of CaMK II could be a new way for the therapy of warm ischemia-reperfusion injury after LT in future clinical practice.
