Correction: Zhang et al. Deficiency of S100A9 Alleviates Sepsis-Induced Acute Liver Injury through Regulating AKT-AMPK-Dependent Mitochondrial Energy Metabolism. Int. J. Mol. Sci. 2023, 24, 2112

Abstract

In the original publication [...].

Figure 4

Inhibition of AMPK reverses S100A9-KO-mediated protection of CLP-induced liver dysfunction. (A) Diagram of AMPK inhibitor Compound C (CC). (B) Schematic diagram of WT or S100A9-knockout (KO) mice treated with CC and CLP operation for 24 h. (C) The levels of serum ALT and AST in each group (n = 6). (D) H&E staining of liver sections (left), and quantification of the histological score (right, n = 6). (E) TUNEL (red) and DAPI (blue) staining of liver sections (left), and quantification of TUNEL⁺ nuclei (right, n = 6). (F) Immunohistochemical staining of liver sections with anti-CD68 antibody (left), and quantification of the CD68⁺ area (right, n = 6). (G) DHE staining of liver sections to measure superoxide production (left), and quantification of fluorescence intensity (right, n = 6). Data are shown as mean ± SEM, and n represents the number of mice in each group.