Research Article

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

Figure 1

The apelin/APJ axis was shut down after random flap operation. (a, c) Western blot results of skin tissue suggest that apelin, APJ, CD34, VEGF, SOD2, and HO-1 were significantly downregulated and apoptosis was upregulated (Bcl2 decreased while Bax increased) after random flap operation. (b, d) IHC staining indicated that the apelin- and APJ-positive area almost halved (scale bar: 50 μm). (e) Immunofluorescence colocalization showed that the codistribution of apelin and APJ in skin microvessels decreased significantly after operation (scale bar: 25 μm). The densitometric analysis of all Western blot bands was normalized to GAPDH. independent experiments. “” means compared with the normal control group. , .
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