Hepatoprotective effect of Cocculus hirsutus on bile duct ligation-induced liver fibrosis in Albino Wistar rats

Background: The aim of this study was to evaluate the potential inhibiting effects of vitamin C as an antioxidant against liver fibrosis and lipid peroxidation in the bile duct ligation- induced biliary obstruction of Wistar rats.Methods: A total of 25 male Wistar albino rats were divided into five groups: sham operated, control (bile duct ligation/BDL) without given vitamin C, BDL with vitamin C 75 mg, BDL with vitamin C 150 mg, and BDL with vitamin C 225 mg. Each group contained 5 animals. Vitamin C was given orally on day 3 after operation and after 14 days following vitamin C administration, all animals were performed laparotomy to obtain liver tissue samples for histopathological investigation of liver fibrosis and blood samples for malondialdehyde (MDA) as lipid peroxidation measurement.Results: The changes demonstrating hepatic fibrosis including moderate to markedly thickened wall of central veins, localized to diffuse perisinusoidal fibrosis, enlarged portal track, increased number of septa, and thickened width of septa were observed in BDL groups. MDA measurement were also observed in all groups. Treatment of biliary obstruction in BDL groups with vitamin C given orally attenuated liver damage. Both the MDA measurement and histopathologic investigation of hepatic fibrosis were observed to be reduced with the vitamin C treatment.Conclusions: Our data indicate that vitamin C inhibited liver fibrosis and lipid peroxidation in bile duct ligation-induced biliary obstruction of Wistar rats.

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Faculty Opinions recommendation of A contradictory role of A1 adenosine receptor in carbon tetrachloride- and bile duct ligation-induced liver fibrosis in mice.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1345984.817085 ◽

2009 ◽

Author(s):

Jonathan A Dranoff

Keyword(s):

Carbon Tetrachloride ◽

Bile Duct ◽

Liver Fibrosis ◽

Adenosine Receptor ◽

Bile Duct Ligation ◽

A1 Adenosine Receptor ◽

Duct Ligation

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Adenoviral CCN3/NOV gene transfer fails to mitigate liver fibrosis in an experimental bile duct ligation model because of hepatocyte apoptosis

Liver International ◽

10.1111/j.1478-3231.2012.02837.x ◽

2012 ◽

Vol 32 (9) ◽

pp. 1342-1353 ◽

Cited By ~ 14

Author(s):

Erawan Borkham-Kamphorst ◽

Sebastian Huss ◽

Eddy Leur ◽

Ute Haas ◽

Ralf Weiskirchen

Keyword(s):

Bile Duct ◽

Gene Transfer ◽

Liver Fibrosis ◽

Bile Duct Ligation ◽

Hepatocyte Apoptosis ◽

Duct Ligation

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PAI-1 deficiency reduces liver fibrosis after bile duct ligation in mice through activation of tPA

FEBS Letters ◽

10.1016/j.febslet.2007.05.049 ◽

2007 ◽

Vol 581 (16) ◽

pp. 3098-3104 ◽

Cited By ~ 56

Author(s):

Hongtao Wang ◽

Yan Zhang ◽

Robert O. Heuckeroth

Keyword(s):

Bile Duct ◽

Liver Fibrosis ◽

Bile Duct Ligation ◽

Duct Ligation ◽

Pai 1

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Polyphenols from Camellia sinenesis attenuate experimental cholestasis-induced liver fibrosis in rats

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00008.2003 ◽

2003 ◽

Vol 285 (5) ◽

pp. G1004-G1013 ◽

Cited By ~ 59

Author(s):

Zhi Zhong ◽

Matthias Froh ◽

Mark Lehnert ◽

Robert Schoonhoven ◽

Liu Yang ◽

...

Keyword(s):

Bile Duct ◽

Liver Fibrosis ◽

Transforming Growth Factor ◽

Bile Duct Ligation ◽

Smooth Muscle Actin ◽

Control Diet ◽

Free Radical Scavengers ◽

Bile Duct Proliferation ◽

Duct Ligation ◽

Experimental Cholestasis

Accumulation of hydrophobic bile acids during cholestasis leads to generation of oxygen free radicals in the liver. Accordingly, this study investigated whether polyphenols from green tea Camellia sinenesis, which are potent free radical scavengers, decrease hepatic injury caused by experimental cholestasis. Rats were fed a standard chow or a diet containing 0.1% polyphenolic extracts from C. sinenesis starting 3 days before bile duct ligation. After bile duct ligation, serum alanine transaminase increased to 760 U/l after 1 day in rats fed a control diet. Focal necrosis and bile duct proliferation were also observed after 1–2 days, and fibrosis developed 2–3 wk after bile duct ligation. Additionally, procollagen-α1(I) mRNA increased 30-fold 3 wk after bile duct ligation, accompanied by increased expression of α-smooth muscle actin and transforming growth factor-β and the accumulation of 4-hydroxynenonal, an end product of lipid peroxidation. Polyphenol feeding blocked or blunted all of these bile duct ligation-dependent changes by 45–73%. Together, the results indicate that cholestasis due to bile duct ligation causes liver injury by mechanisms involving oxidative stress. Polyphenols from C. sinenesis scavenge oxygen radicals and prevent activation of stellate cells, thereby minimizing liver fibrosis.

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Vitamin D inhibits development of liver fibrosis in an animal model but cannot ameliorate established cirrhosis

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00132.2013 ◽

2015 ◽

Vol 308 (2) ◽

pp. G112-G120 ◽

Cited By ~ 37

Author(s):

Shirley Abramovitch ◽

Efrat Sharvit ◽

Yosef Weisman ◽

Amir Bentov ◽

Eli Brazowski ◽

...

Keyword(s):

Vitamin D ◽

Growth Factor ◽

Bile Duct ◽

Liver Fibrosis ◽

Bile Duct Ligation ◽

Active Form ◽

Preventive Treatment ◽

Antifibrotic Effect ◽

Duct Ligation

1,25(OH)2D3, the active form of vitamin D, has an antiproliferative and antifibrotic effect on hepatic stellate cells. Our aim was to investigate the potential of 1,25(OH)2D3 to inhibit the development of liver fibrosis and to ameliorate established fibrosis in vivo. The antifibrotic effect of 1,25(OH)2D3 was investigated in a thioacetamide (TAA) model (as a preventive treatment and as a remedial treatment) and in a bile duct ligation model. In the preventive model, rats received simultaneously intraperitoneum injection of TAA and/or 1,25(OH)2D3 for 10 wk. In the remedial model, rats were treated with TAA for 10 wk and then received 1,25(OH)2D3 or saline for 8 wk. Fibrotic score was determined by Masson staining. Collagen I, α-smooth muscle actin (α-SMA), tissue inhibitor of metalloproteinase-1 (TIMP1), platelet-derived growth factor (PDGF), and transforming growth factor-β (TGF-β) expression were measured by Western blot analysis and real-time PCR. Hypercalemia was detected by chemistry measurements. Preventive treatment of 1,25(OH)2D3 significantly suppressed liver fibrosis both macroscopically and microscopically and significantly lowered the fibrotic score of the TAA + 1,25(OH)2D3 group compared with the TAA group. 1,25(OH)2D3 significantly inhibited expression of PDGF and TGF-β by ∼50% and suppressed the expression of collagen Iα1, TIMP1, and α-SMA by approximately three-, two-, and threefold, respectively. In contrast, 1,25(OH)2D3 was inefficient in amelioration of established liver fibrosis. Administration of 1,25(OH)2D3 to bile duct ligation rats led to a high mortality rate probably caused by hypercalcemia. We conclude that 1,25(OH)2D3 may be considered as a potential preventive treatment in an in vivo model but failed to ameliorate established cirrhosis.

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