To explore the mechanism of emodin in reducing ALT and CA19-9 levels in hepatobiliary damp-heat cholestasis based on FXR signaling pathway

Abstract

Objective : To further explore the therapeutic effect and mechanism of emodin on acute cholestatic hepatitis model rats. Method:  The 96 Mice were divided into 5 groups: emodin group, ursodeoxycholic acid group, dexamethasone group, model group, normal control group, 24 mice in each. Except for the normal control group, in the 5th-day gastric perfusion of alpha-naphthyl isothiocyanate ( ANIT) of naphthyl isothiocyanate to establish an animal model of cholestatic hepatitis, and given appropriate drug interventions. Specimens were collected at 24, 48, and 723-time points after modelling (8 animals per time point) to detect liver function and liver pathology. Real-time fluorescence quantitative detection of cytokine-induced neutrophil chemokine 1 macrophage Detection of Intercellular Adhesion Molecule Protein Expression in Liver Tissue by Western blot. 24 rats were treated as control. Result: Flavin group 24, 48, 72 h Total bilirubin at each time point [starvation, ( 32. 8 ± 3. 7)µmol/L, ( 61. 0 ± 16. 4 ) µmol/L, (10.8 ± 4.5) µmol/L , direct bilirubin ( 26.03 ± 3.10) µmol/L, ( 49.40 ± 18.16) µmol/L, ( 8.04 ± 3.03) µmol/L ], alanine aminotransferase [(314 ± 50) U/L, (664 ± 97) U/L, (200 ±60) U/L] significantly lower. The emodin group TBA level was significantly lower than the ursodeoxycholic group (P<0.05). MIP-2 and CINC-1 expression levels at all-time point emodin group significantly lower than the model group (P<0.005). AT different time points emodin group was significantly lower than the other groups. Conclusion: Flavin treatment of eight ANIT, PB, DB, ALT expression levels were significantly lower than those of acute cholestatic hepatitis model rats induced at the same time. Most significantly, the onset of action is faster than that of ursodeoxycholic acid, and its effect on ALT, AST, GGT, and TBA is better than that of dexamethasone.  The mechanism may be related to the inhibition of the activation of CINC-1, MIP-2, and ICAM-1.