Effects Of Sevoflurane Precondionting On Caspase-3 And Bcl-2 After Focal Cerebral Ischemia-reperfusion In Rats

PURPOSE: Clinically, cerebral ischemia reperfusion injury in patients can affect the outcome of the disease, even endanger the lives of patients, resulting in irreparable losses. Currently, the pathogenesis of the cerebral ischemia reperfusion injury has not been entirely explained. Apoptosis which is one of the main patterns of neuronal death plays an important role in cerebral isehemia-reperfusion indueced injury. The expression of caspase-3 which is a apoptosis inducer and Bcl-2 which is a apoptosis inhibitor is closely related to the apoptosis. Sevoflurane as a new volatile anaesthetie is widely used in clinical. Some studies show that sevoflurane has an ischemic preconditioning effect. This experiment is based on cerebral ischemia-reperfusion model. We observe the sevoflurane's effect on the expression of Caspase-3 and Bcl-2 after preconditioning by sevoflurane. and explained the effects of sevoflurane against focal ischemia reperfusion induced injury from the perspective of apoptosis, and the possible mechanism of anti-apoptosis too.METHOD: We established right middle cerebral artery occlusion(MCAO) model based on Zea Longa method. Twenty-four Wistar male rats were randomly divided into three groups: sham operation group(S n=8), ischemia reperfusion group (A n=8) and sevoflurane preconditioning group (B n=8). We established right middle cerebral artery occlusion (MCAO) model based on Zea Longa method twenty-four hours after reperfusion. Apoptosis were determined by Hematoxylin and Eosin (HE), and the expression of caspase-3 and Bcl-2 by immunohistochemistry.RESULTS: 1. HE staining: the structure and hierarchy in sham operation group of hippocampal neurons are clear. There are many typical apoptosis cells in the hippocampal in ischemia reperfusion group. Apoptosis cells in sevoflurane preconditioning group distribute relatively decreased. 2. Caspase-3 immunohistochemistry show that Caspase-3 expression increased (p<0.01) after cerebral ischemia. Sevoflurane preconditioning can inhibit the upregulation of its expression (p<0.05) 3. Bcl-2 immunohistochemistry shows that Bcl-2 expression increased after cerebral ischemia reperfusion, compare with sham operation group(p<0.01) . Sevoflurane preconditioning group compared with the ischemia reperfusion group, Bcl-2 was not obvious increased(p> 0.05).CONCLUSION: 1. There is apoptosis when ischemia reperfusion occurs, sevoflurane preconditioning can inhibit apoptosis. 2. Sevoflurane preconditioning can not increase the expression of Bcl-2, the effect of its ischemic preconditioning may not be by promoting the expression of Bcl-2. 3. Sevoflurane can inhibit the expression of Caspase-3, which may be a mechanism of its effect that reduced neuronal apoptosis when cerebral ischemia reperfusion occurs.