α7 Nicotinic Acetylcholine Receptor Mediates the Neuroprotection of Remote Ischemic Postconditioning in a Rat Model of Asphyxial Cardiac Arrest.

摘要: Abstract Background Remote ischemic postconditioning (RIPost) has been shown to reduce the ischemia–reperfusion injury of heart and brain. However, protection mechanisms have not yet fully elucidated. We observed that RIPost could alleviate brain after cardiac arrest (CA). The aim this study was explore whether α7 nicotinic acetylcholine receptor (α7nAChR) mediates neuroprotection in a rat model asphyxial CA. Materials methods Asphyxial CA induced by occlusion tracheal tube for 8 min resuscitated later. produced three cycles 15-min release right hind limb tourniquet performed respectively at moment third hour restoration spontaneous circulation. α7nAChR agonist PHA-543613 antagonist methyllycaconitine (MLA) were used investigate role mediating neuroprotective effects. Results showed decreased hippocampus cortex resuscitation, whereas attenuate reduction. use provided effects against cerebral Furthermore, levels neuron-specific enolase, inflammatory mediators, number apoptotic cells, phosphorylation nuclear factor-κB while increased signal transducer activator transcription-3. above attenuated methyllycaconitine. Conclusions Neuroprotection related with activation α7nAChR, which suppress activate transcription-3 model.