F4/80 Antibody - #DF2789

Figure 2 Hepatic asprosin deficiency alleviates hepatic steatosis. a) Schematic illustration of the experimental design employed to assess the impact of hepatic asprosin deficiency on hepatic steatosis. b) Liver weight, and LW/BW of C57BL/6J mice from different groups. n = 8 in each group. c) AAV-shAsprosin reduced the elevated serum transaminase level induced by HFCDAA feeding in C57BL/6J mice. n = 6–8 in each group. d) The total cholesterol and triglyceride content of the livers. n = 8 in each group. e,f) The serum TG, TC, LDL, HDL levels. n = 8 in each group. g,h) Representative histological sections stained with Oil Red O, hematoxylin and eosin (H&E), and Masson's trichrome. Quantitative analyses of Oil Red O positive areas, non-alcoholic fatty liver disease activity score (NAS), and detection of liver hydroxyproline content are shown. n = 6–8 in each group. i,j) Immunohistochemical staining for CD68 and immunostaining staining for F4/80. Quantitative of CD68 positive areas and mean fluorescence intensity of F4/80 staining are shown. n = 5–7 in each group. k) AAV-shAsprosin changed the expression of genes involved in lipid metabolism. n = 6–8 in each group. l) Schematic illustration of the experimental design employed to assess the impact of adipose asprosin deficiency on hepatic steatosis. m) Representative histological sections stained with Oil Red O, hematoxylin, and eosin (H&E). n = 6 in each group. n) The serum ALT, AST levels. n = 6 in each group. LW/BW, liver weight/body weight, TC, total cholesterol; TG, triglyceride; ALT, aspartate aminotransferase; AST, alanine aminotransferase; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; ND, normal diet; HFCDAA, high fat, methionine choline deficiency diet. Scale bar for Oil Red O, H&E, Masson's trichrome staining, and CD68 immunohistochemical: 50 µm, for F4/80 immunostaining: 100 µm. Statistical analysis was performed with one-way ANOVA. **p < 0.01 versus ND+AAV-shNC. #p < 0.05, ##p < 0.01 versus HFCDAA+AAV-shNC.

Figure 1 LPS/D-GalN-induced ALF enhances apoptosis and ferroptosis. (A) The survival rate of WT mice treated with vehicle or LPS/D-GalN (LPS, 20 μg/kg; D-GalN, 700 mg/kg) (n = 10). (B) Representative pictures of WT mice treated with vehicle or LPS/D-GalN for 3, 5, and 6 hours (n = 10). (C) Serum levels of ALT and AST with or without LPS/D-GalN co-injection (n = 6). (D) H&E and TUNEL staining after LPS/D-GalN co-injection (n = 6). (E) Immunohistochemistry of TNFα and F4/80 staining after LPS/D-GalN co-injection (n = 6). (F) Transmission electron microscope of liver tissues (n = 3). (G) MDA assay of liver homogenates (n = 5). (H and J) Western blot analyses of TFR, DMT1, GPX4, and XCT from WT mice (H) with or without LPS/D-GalN and (I) quantitative results (n = 3–9). (I and K) FSP1, DHODH, and POR proteins. Western blot analyses of WT mice (I) with or without LPS/D-GalN and (K) quantitative results (n = 3–9). (L) Immunohistochemistry of DMT1 staining and immunofluorescence of Ptgs2 in livers with or without LPS/D-GalN (n = 6). (M) Quantitative results of DMT1 and Ptgs2. All data were obtained from WT mice. Scale bars: 100 μm. Data are presented as means ± SEM. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001. DAPI, 4′,6-diamidino-2-phenylindole; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.