Figure 3.

IL-22 prevents generation of dysfunctional mitochondria and mitochondrial ROS via AMPK-associated signal mechanism. Hepatocytes were treated with PBS, 200 mM ethanol, or 5 μg/mL cisplatin, or 0.25 mM palmitic acid, or 10 mM CCl₄ in the absence or presence of IL-22 for 24 h (n = 3) (A) Mitochondrial mass was stained with MitoTracker Green and assessed by flow cytometry. Mitochondrial ROS and membrane potential were assessed in hepatocytes stained with MitoSOX (C), MitoTracker Green and MitoTracker Red (B), or MitoTracker Green and MitoSOX (D), respectively. (E) Confocal images indicated mitochondrial ROS production in hepatocytes stained with MitoSOX. (F) Western blot analysis suggested that IL-22 induced AMPK/AKT activation in hepatocytes, which could be inhibited by Dorsomorphin. (G) OCR in hepatocytes was measured in the absence or presence of indicated inhibitors and IL-22 for 24 h. Student's t test (unpaired); *P < 0.05, **P < 0.01, ***P < 0.001. All data are means ± SD of at least three independent experiments.