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Figure 2.Sustained PHLPP-1 attenuated insulin-activated Akt phosphorylationYoung and aged rats were subjected to sham, 30 minutes of in vivo ischemia and followed by 30 minutes of reperfusion with or without insulin treatment (60 U/L, intravenous infusion at 4 mL/kg per h for 30 minutes, beginning 5 min before reperfusion) and then hearts were collected for Western blots. (A) Representative immunoblots showing PHLPP-1 content and phosphorylation of Akt at Ser473 from heart extracts of young and aged rats. The bar graphs show the relative levels of PHLPP-1 (B) and phosphorylation of Akt at Ser473 (C), respectively (*P < 0.05 vs. Young sham; #P < 0.05 vs. Young I/R; P < 0.05 vs. Young I/R+Ins. Values are means ± S.E., n = 5 per group).
Figure 2 — Mutual inhibition of insulin signaling and PHLPP-1 determines cardioprotective efficiency of Akt in aged heart | Aging