Fig 1: Increase in CXCL14 expression is associated with the intensity of hepatitis in mice in MHV‐3‐induced fulminant hepatitis model. Mice were injected intraperitoneally either with DPBS (Mock) or with MHV‐3. 72 h after, mice were euthanized to collect the liver and the serum. (A) H&E staining (left) and cleaved‐caspase 3 immunolabeling (right) in the livers of control (Mock) and MHV‐3‐infected mice (72 hpi). (B) ALT levels in the sera of control (Mock) and MHV‐3‐infected mice (72 hpi). Gray area is the normal range of ALT observed in non‐treated mice. (C) Titration of CXCL14 in the sera of control (Mock) and MHV‐3‐infected mice by ELISA (72 hpi). (D) Exponential correlation curve between ALT and CXCL14 levels in the sera of MHV‐3‐infected mice 72 hpi. A p‐value < 0.05 was considered significant: **< 0.01, ***< 0.001 (comparison between Mock mice and MHV‐3 infected mice).
Fig 2: FC was positively correlated with hepatic injury in both NAFLD patients and mice. (A) Plasma levels of TC, FC, CE and ALT in human. (B) Correlation analysis between ALT value and TC, FC or CE levels in human. (C) Plasma levels of TC, FC, CE and ALT in mice. (D) Hepatic levels of TC, FC, CE and ALT in mice. (E‐F) Correlation analysis between ALT value and TC, FC or CE levels in mice plasma (E) and liver (F).
Fig 3: Effects of ESF on ethanol-induced liver injury. (a) H&E-stained liver sections of EtOH-induced liver injury model. The droplets are indicated by the black arrow. All images are visualized at 100×, (n = 10). (b) Liver/BW (%). (c) Activities of AST in serum. (d) Activities of ALT in serum. Data are shown as the mean ± SEM (n = 10). Statistical analyses were different values according to the one-way ANOVA with Tukey’s range test (Normal diet vs. EtOH diet ### p < 0.001; EtOH diet vs. EtOH diet + ESF or silymarin *** p < 0.001, ** p < 0.01).
Fig 4: Elevated CXCL14 levels in the sera of patients with acute viral hepatitis. Serum of patients with acute hepatitis and healthy donors were collected to measure CXCL14 concentration and transaminase levels. (A) Quantification of CXCL14 in the sera of healthy donors, patients with non‐viral hepatitis, and patients with viral hepatitis. (B) Quantification of CXCL14 in the sera of healthy donors and patients with viral hepatitis, depending on the virus causing the hepatitis. (C) Correlation between CXCL14 concentration and ALT activity in the sera of patients with acute viral hepatitis, according to the virus. (D) ROC curve of CXCL14 in the group of patients with viral hepatitis (left) or non‐viral hepatitis (right). AUC and p‐value are shown on the graph. A p‐value < 0.05 was considered significant: ***< 0.001, ****<0.0001 (comparison between healthy donors and acute hepatitis patients).
Fig 5: ER stress response following hepatic AAV8-coF8 gene transfer declines over time in C57BL/6 mice. (a) Systemic levels of FVIII antigen as a function of time in C57BL/6 mice (n = 5) injected with 1 × 1011 vg of an AAV8-coF8 vector. (b) Anti-FVIII IgG1 levels in plasma at 12 weeks. (c) Liver enzyme levels (ALT, alanine transaminase) in plasma 12 weeks after hepatic gene transfer. Dotted lines represent mean ± 1 SD of ALT measured in naive C57BL/6 mice. (d) Analysis of the expression status of UPR chaperones as a consequence of hepatic gene transfer of coF8 in C57BL/6 mice 12 weeks post-treatment. Western Blotting of liver tissue lysates for detection of BiP, CHOP, and actin in C57BL/6 mice (n = 5) receiving 1 × 1011 vg. For additional comparison, protein extract from a C57BL/6 mouse treated with tunicamycin (T) or that was untreated (N, “naive”). AAV, adeno-associated virus; BiP, binding immunoglobulin protein; CHOP, CCAAT/enhancer-binding protein homologous protein; ER, endoplasmic reticulum; FVIII, functional factor VIII; UPR, unfolded protein response.
Supplier Page from Abcam for Alanine Transaminase Activity Assay Kit (Colorimetric/Fluorometric)