FIGURE 4.

IL‐22 maintains mitochondrial integrity and cellular metabolism of TECs via induction of PFKFB3. (A) Volcano plot for genes expression in TECs stimulated with glucose, or cisplatin, or palmitic acid, or CCl₄ in the presence or absence of IL‐22 for 24 h. (B) Confocal microscopic data demonstrated PFKFB3 overexpression in TECs after IL‐22 treatment, which required AMPK/AKT signaling activation. (C) Real‐time PCR results indicating that IL‐22 induced PFKFB3 overexpression in TECs, which could be inhibited by AMPK/AKT signaling blocked. (D) The AMPK/AKT/ PFKFB3 signaling pathway activation in TECs after treated with Compound C and LY294002. (E and F) ECAR and OCR in TECs at the presence or absence of IL‐22, or si‐PFKFB3 for 24 h. (G) Glucose consumption in TECs after IL‐22 or si‐PFKFB3 treatment for 24 h. (H) Mitochondrial dysfunction was evaluated in TECs stained with MitoTracker Red and MitoTracker Green. Student's t‐test (unpaired); n = 3; ***p < 0.001, **p < 0.01, *p < 0.05