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. 2020 Apr 27;10(13):5879–5894. doi: 10.7150/thno.43894

Figure 6.

Figure 6

IL-22 attenuates hepatic oxidative stress, mitochondrial dysfunction and damage in vivo. (A) Schematic diagram of the animal experimental protocols to assess the effects of IL-22 (0.5 mg/kg and 1.5 mg/kg) in cisplatin (20 mg/kg) induced liver injury. N-acetyl-L-cysteine (NAC, 150 mg/kg) as a positive control group and PBS as a vehicle control group (n = 5). Representative HE (B), MitoSOX (E), JC-1 (F), and Ki-67 staining (G) images of the liver sections were presented. (C and D) Serum AST levels, serum ALT levels, liver weights and spleen weights were measured (H) Comparison of AMPK/AKT/mTOR activation in liver extracts from IL-22-treated mice versus control subjects was assessed by western blot analysis. (I) Schematic diagram of the animal experimental protocols to assess the effects of IL-22 (2.5 mg/kg) in high-fat-diet fed mice (n = 8). PBS treated mice as a vehicle control group (n = 5). (J) Representative HE, MitoSOX, and JC-1 staining images of the liver sections were presented. (K) Liver extracts were subjected to western blot analysis with various antibodies as indicated. Western blotting suggested that IL-22 induced AMPK/AKT/mTOR activation in liver extracts from IL-22-treated mice. (L) The mRNA expression levels of the indicated genes in the liver (n = 3). Student's t test (unpaired); *P ≤ 0.05 and **P ≤ 0.01 compared with cisplatin-treated and HFD-fed mice. #P ≤ 0.05 and ##P ≤ 0.01 compared with PBS-treated and chow diet fed mice. All data are means ± SD of at least three independent experiments.