The role of XXXX release on voltage-dependent anion channels (VDAC)-mediated apoptosis in an eleven vessel occlusion model in @entity35 .

@entity10740 @entity2227 @entity63 @entity2310 @entity35
Voltage-dependent anion channel (VDAC) is the main protein in mitochondria-mediated apoptosis, and the modulation of VDAC may be induced by the excessive release of extracellular @entity2227 . This study examined the role of @entity2227 release on VDAC-mediated apoptosis in an eleven vessel occlusion model in @entity35 . Male @entity35 (250-350 g) were used for the 11 vessel occlusion @entity63 model, which were induced for a 10-min transient occlusion. During the @entity63 and initial reperfusion episode, the real-time monitoring of the extracellular @entity2227 concentration was measured using an amperometric microdialysis biosensor and the cerebral blood flow (CBF) was monitored by laser-Doppler flowmetry. To confirm neuronal apoptosis, the brains were removed 72 h after @entity63 to detect the neuron-specific nuclear protein and pro-apoptotic proteins (cleaved caspase-3, VDAC, @entity10740 and @entity2310 ). The changes in the mitochondrial morphology were measured by atomic force microscopy. A decrease in the % of CBF was observed, and an increase in @entity2227 release was detected after the onset of @entity63 , which continued to increase during the @entity63 period. A significantly higher level of @entity2227 release was observed in the @entity63 group. The increased @entity2227 levels in the @entity63 group resulted in the activation of VDAC and pro-apoptotic proteins in the hippocampus with morphological alterations to the mitochondria. This study suggests that an increase in @entity2227 release promotes VDAC-mediated apoptosis in an 11 vessel occlusion @entity63 model.
