Apelin/APJ-Manipulated CaMKK/AMPK/GSK3β Signaling Works as an Endogenous Counterinjury Mechanism in Promoting the Vitality of Random-Pattern Skin Flaps

Figure 4

Apelin13 enhanced random flaps’ viability through AMPK/GSK3β signaling in vivo and in vitro. (a) Western blot bands suggested phosphorylation difference of GSK3β and AMPK between normal skin and random flap. (b) Ratio of phosphorylated AMPK/total AMPK and phosphorylated GSK3β/total GSK3β. (c–e) Phosphorylation of AMPK and GSK3β in all groups after apelin13 with or without ML221 in vivo. (f–h) Phosphorylation of AMPK and GSK3β in all groups after apelin13 with or without ML221 in vitro. The densitometric analysis of all Western blot bands was normalized to total protein and GAPDH. independent experiments. “” means compared with the normal control group; “#” means compared with the random flap group (or OGD/R group); “@” means compared with the random flap+apelin13 group (or OGD/R+apelin13 group). , .

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