Abstract
Bicyclol and silymarin are widely used in the treatment of various liver diseases; however, there is no report on comparative effect of them on liver fibrosis. To compare their liver protective effect, liver fibrosis rats induced by bile duct ligation (BDL) were orally treated with 100 mg/kg bicyclol and 100 mg/kg silymarin respectively for 4 weeks. Liver index, liver function activities, inflammatory biomarkers, fibrotic biomarkers and liver histopathology were assessed. BDL induced marked histopathological changes in liver tissues coupled with changes in serum biochemistry. Furthermore, hepatic content of hydroxyproline, transforming growth factor-beta1 (TGF-β1), and interleukin-6 (IL-6) were elevated, together with a reduction of interleukin-1 alpha (IL-1α) and interleukin-4 (IL-4) in the liver. In addition, BDL increased the expression of alpha-smooth muscle actin (α-SMA). Treatment with bicyclol or silymarin protected against BDL induced liver fibrosis, as proved by the alleviation of inflammatory and fibrotic biomarkers. Overall, our results indicated that the effect of bicyclol was better than that of silymarin. Key words: Liver fibrosis, bile duct ligation, bicyclol, silymarin, comparative effect.  
Highlights
Several chronic inflammatory diseases, such as viral hepatitis, alcoholic and primary biliary cirrhosis, might result in liver fibrosis
After 4 weeks, the liver index of the bile duct ligation (BDL) rats significantly increased, reaching 185.7% of that in the sham control and it was antagonized by treatment with silymarin or bicyclol to 71.2 and 61.3%, respectively (Figure 2)
The serum levels of ALT, AST, alkaline phosphatase (ALP), gamma glutamyl transpeptidase (GGT), total bilirubin (TBIL), and direct bilirubin (DBIL) were increased significantly, whereas the level of ALB and the albumin to globulin ratio (A/G) was decreased significantly in BDL rats compared with sham control
Summary
Several chronic inflammatory diseases, such as viral hepatitis, alcoholic and primary biliary cirrhosis, might result in liver fibrosis. This pathology is characterized by excessive deposition of extracellular matrix (ECM) components in response to acute chronic liver injury. Accumulation of ECM proteins distort the hepatic architecture by the formation of a fibrous scar, nodules of regenerating hepatocytes and pathologic angiogenesis, leads to cirrhosis (Gulamhusein and Hirschfield, 2019; Schutte et al, 2013).
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