Apelin-13 protects against apoptosis by activating XXXX -activated protein kinase pathway in @entity63 stroke.

@entity1380 @entity2806 @entity63 @entity19 @entity8582 @entity1379
UNASSIGNED: Apelin has been proved to be protective against apoptosis induced by ischemic reperfusion. However, mechanisms whereby apelin produces neuroprotection remain to be elucidated. @entity8582 -activated protein kinase (AMPK) is a master energy sensor that monitors levels of key energy metabolites. It is activated via AMPKaThr172 phosphorylation during @entity2806 and appears to be neuroprotective. In this study, we investigated the effect of apelin on AMPKa and tested whether apelin protecting against apoptosis was associated with AMPK signals. Focal transient @entity2806 /reperfusion (I/R) model in male ICR @entity19 was induced by 60min of @entity63 followed by reperfusion. Apelin-13 was injected intracerebroventricularly 15min before reperfusion. AMPK inhibitor, compound C, was injected to @entity19 intraperitoneally at the onset of @entity63 . In experiment 1, the effect of apelin-13 on AMPKa was measured. In experiment 2, the relevance of AMPKa and apelin-13' effect on apoptosis was measured. Data showed that apelin-13 significantly increased AMPKa phosphorylation level after cerebral I/R. Apelin-13, with the co-administration of saline, reduced apoptosis cells, down-regulated @entity1380 and cleaved-caspase3 and up-regulated @entity1379 . However, with the co-administration of compound C, apelin-13 was inefficient in affecting apoptosis and @entity1380 , @entity1379 and cleaved-caspase3. The study provided the evidence that apelin-13 up-regulated AMPKa phosphorylation level in @entity2806 insults and AMPK signals participated in the mechanism of apelin-mediated neuroprotection.
