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

Figure 2

Apelin13 treatment promoted the viability of a random flap. (a) Digital photographs of flap appearances of the random flap group, random flap+apelin13 group, and random flap+apelin13+ML221 groups on day 1, day 3, and day 7 and their inner side photos on day 7 were recorded. (b) The percentages of the survival area and edema degree in three groups were quantified and analyzed. (c) Full-field LDBF images of flaps in each group on day 3, day 5, and day 7. (d) A schematic diagram of a rectangular area () of surgery and scanning. (e) The signal intensity of blood flow of flaps was quantified and analyzed. (f) HE staining showed vessels in area II of flaps in all groups (original magnifcation×200; scale bar: 50 μm). IHC staining showed CD34-positive vessels in area II in all groups (original magnification ×200; scale bar: 50 μm). (g) Histogram of mean vessel density and CD34-positive vessel density in each group. Western blot bands of apoptosis indexes (h), antioxidant stress proteins (i), and statistical results (j). The densitometric analysis of all Western blot bands was normalized to GAPDH. Antioxidant enzymes such as CAT and GSH and oxidative marker carbonylated protein levels in all groups of random flaps were measured (k). independent experiments. “” means compared with the normal control group; “#” means compared with the random flap group; “@” means compared with the random flap+apelin13 group. , .

(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)

(i)

(j)

(k)