Sie befinden Sich nicht im Netzwerk der Universität Paderborn. Der Zugriff auf elektronische Ressourcen ist gegebenenfalls nur via VPN oder Shibboleth (DFN-AAI) möglich. mehr Informationen...
Ergebnis 18 von 6085

Details

Autor(en) / Beteiligte
Titel
Apelin-13 protects against apoptosis by activating AMP-activated protein kinase pathway in ischemia stroke
Ist Teil von
  • Peptides (New York, N.Y. : 1980), 2016-01, Vol.75, p.96-100
Ort / Verlag
United States: Elsevier Inc
Erscheinungsjahr
2016
Quelle
MEDLINE
Beschreibungen/Notizen
  • •Apelin-13 increased AMPKα phosphorylation level after cerebral ischemia/reperfusion.•Apelin-13 has minimal effect on attenuating apoptosis when AMPKα was inhibited.•Apelin-13 was ineffective on Bax, Bcl-2 and caspase-3 with AMPK inhibitor. Apelin has been proved to be protective against apoptosis induced by ischemic reperfusion. However, mechanisms whereby apelin produces neuroprotection remain to be elucidated. AMP-activated protein kinase (AMPK) is a master energy sensor that monitors levels of key energy metabolites. It is activated via AMPKαThr172 phosphorylation during cerebral ischemia and appears to be neuroprotective. In this study, we investigated the effect of apelin on AMPKα and tested whether apelin protecting against apoptosis was associated with AMPK signals. Focal transient cerebral ischemia/reperfusion (I/R) model in male ICR mice was induced by 60min of ischemia followed by reperfusion. Apelin-13 was injected intracerebroventricularly 15min before reperfusion. AMPK inhibitor, compound C, was injected to mice intraperitoneally at the onset of ischemia. In experiment 1, the effect of apelin-13 on AMPKα was measured. In experiment 2, the relevance of AMPKα and apelin-13′ effect on apoptosis was measured. Data showed that apelin-13 significantly increased AMPKα phosphorylation level after cerebral I/R. Apelin-13, with the co-administration of saline, reduced apoptosis cells, down-regulated Bax and cleaved-caspase3 and up-regulated Bcl2. However, with the co-administration of compound C, apelin-13 was inefficient in affecting apoptosis and Bax, Bcl2 and cleaved-caspase3. The study provided the evidence that apelin-13 up-regulated AMPKα phosphorylation level in cerebral ischemia insults and AMPK signals participated in the mechanism of apelin-mediated neuroprotection.

Weiterführende Literatur

Empfehlungen zum selben Thema automatisch vorgeschlagen von bX