Fig. 1: Increased HO-1 expression is involved in pathological changes in CLI.
From: Activation of Nrf2/HO-1 signaling pathway exacerbates cholestatic liver injury

a Representative H&E staining of liver tissues in mice (6- to 8-week-old) after administration of ZnPP, followed by 295.9 mg/kg OA or 60 mg/kg ANIT (n = 5). Neutrophil infiltration (green arrows) and hepatocyte necrosis (yellow arrows or dashed circles). Scale bar, 100 μm or 50μm. b–g Serum levels of ALT, AST, ALP, TBA, TBIL, and DBIL (n = 5). h Liver UCB concentration (n = 5). i, j Expression of HO-1 protein and mRNA after oral administration of OA (n = 6). k Immunohistochemical staining of liver HO-1. Scale bar, 50 μm. Kupffer cells (green triangles) and hepatocyte (yellow triangles). l Expression of HO-1 protein after intragastric administration of ANIT (n = 5). Student’s t test or nonparametric tests (b–h), and one-way ANOVA (h–j) with Tukey’s post hoc test were used for data analysis. All data are shown as Mean ± SEM. *p < 0.05, **p < 0.01, significant difference compared to the control group; #p < 0.05, ##p < 0.01, significant difference between the OA or ANIT alone group and the ZnPP-combined group. ALP alkaline phosphatase, ALT alanine aminotransferase, ANIT α-naphthylisothiocyanate, AST aspartate aminotransferase, DBIL direct bilirubin, H&E hematoxylin and eosin, HO-1 heme oxygenase-1, OA oleanolic acid, TBA total bile acid, TBIL total bilirubin, ZnPP protoporphyrin IX zinc.