RESUMO
Objective To investigate the effects of adenosine 5'-monophosphate-activated protein kinase (AMPK) and phosphated AMPK (pAMPK) signals in ischemic preconditioning (IPC), and the effect of pharmacological intervention of AMPK on infarct size of the brain. Methods A brief (3min) middle cerebral artery occlusion (MCAO) was employed to induce IPC in male rat, and another 90-min MCAO was performed 4 or 72h later. The levels of AMPK and pAMPK were assessed after IPC. A pharmacological activator metformin, or inhibitor compound C of AMPK, was used to analyze the correlation of IPC to AMPK signaling in MCAO rats. Results The infarct size of total cerebral hemisphere and cortex was significantly decreased in MCAO animals by IPC for 72h (P0.05, n=6). The AMPK activator metformin can significantly reverse the protective effect of IPC (P<0.05, n=6). Conclusions The signals of AMPK and pAMPK play an important role in neuroprotective effect of IPC on cerebral ischemic injury. The neuroprotective effect of IPC may be associated with the down-regulation of pAMPK.