| Autor: |
Zhu J, Rebecchi MJ, Tan M, Glass PS, Brink PR, Liu L, Zhu, Jiang, Rebecchi, Mario J, Tan, Minyi, Glass, Peter S A, Brink, Peter R, Liu, Lixin |
| Zdroj: |
Journals of Gerontology Series A: Biological Sciences & Medical Sciences; Jun2010, Vol. 65A Issue 6, p611-619, 9p |
| Abstrakt: |
Pretreatment with isoflurane decreased myocardial infarction size in young rats (3-5 months) but not in old rats (20-24 months). To understand the mechanisms underlying the failure to protect the old myocardium, differences in phosphorylation of Akt/GSK-3beta and age-associated differences in mitochondrial permeability transition pore (mPTP) opening in the aging heart in vivo were measured. Isoflurane significantly increased Akt and GSK-3beta phosphorylation in the young groups. In contrast, levels of p-Akt and p-GSK-3beta were highly elevated in the old sham control groups. Isoflurane preconditioning significantly reduced the fall in NAD(+) levels induced by ischemia/reperfusion injury in the young animals, reflecting the inhibition of mPTP opening. In the old animals, however, isoflurane failed to prevent the fall in NAD(+) levels induced by ischemia/reperfusion injury. Lack of isoflurane-induced cardioprotective effects, seen in the old animals, can be explained by age-related differences in Akt/GSK-3beta signaling pathway and the inability to reduce mPTP opening following ischemia/reperfusion injury. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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