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Apoptosis,a form of neuronal damage,takes place following cerebral ischemia/reperfusion injury,and caspase-3 plays an important role in apoptosis.Studies have shown that morphine preconditioning influences neuronal apoptosis and related protein expression following cerebral ischemia/reperfusion injury.In the present study,neuronal degeneration was attenuated,and the number of apoptotic cells and caspase-3 expression decreased following morphine preconditioning in a rat model of cerebral ischemia/reperfusion injury.Moreover,pathological changes were attenuated with increasing morphine doses,as well as the number of apoptotic cells and caspase-3 expression.Results from the present study revealed that morphine preconditioning reduced ischemic brain injury and improved cerebral ischemic tolerance in a dose-dependent manner.The anti-apoptotic mechanism of morphine is closely related to Caspase-3.
Apoptosis, a form of neuronal damage, takes place following cerebral ischemia / reperfusion injury, and caspase-3 plays an important role in apoptosis. Studies have shown that morphine preconditioning influencing neuronal apoptosis and related protein expression following cerebral ischemia / reperfusion injury. In the present study, neuronal degeneration was attenuated, and the number of apoptotic cells and caspase-3 expression than following morphine preconditioning in a rat model of cerebral ischemia / reperfusion injury. Moreover, pathological changes were attenuated with increasing morphine doses, as well as the number of apoptotic cells and caspase-3 expression. Results from the present study study that morphine preconditioning reduced ischemic brain injury and improved cerebral ischemic tolerance in a dose-dependent manner. The anti-apoptotic mechanism of morphine is closely related to Caspase-3.