OBJECTIVEThe aim of our study was to assess the complications of hepatic fibrosis associated with bile duct ligation and the potential curative role of sepia ink extract in hepatic damage induced by bile duct ligation.

METHODSRattus norvegicus rats were divided into 3 groups: Sham-operated group, model rats that underwent common bile duct ligation (BDL), and BDL rats treated orally with sepia ink extract (200 mg/kg body weight) for 7, 14, and 28 d after BDL.

RESULTSThere was a significant reduction in hepatic enzymes, ALP, GGT, bilirubin levels, and oxidative stress in the BDL group after treatment with sepia ink extract. Collagen deposition reduced after sepia ink extract treatment as compared to BDL groups, suggesting that the liver was repaired. Histopathological examination of liver treated with sepia ink extract showed moderate degeneration in the hepatic architecture and mild degeneration in hepatocytes as compared to BDL groups.

CONCLUSIONSepia ink extract provides a curative effect and an antioxidant capacity on BDL rats and could ameliorate the complications of liver cholestasis.

Animals ; Antioxidants ; pharmacology ; Bile Ducts ; surgery ; Biomarkers ; blood ; Cholestasis, Extrahepatic ; blood ; etiology ; prevention & control ; Collagen ; metabolism ; Ink ; Liver ; metabolism ; Liver Function Tests ; Male ; Oxidative Stress ; Rats ; Sepia ; chemistry

Objective To compare the degree of ameliorative effects of Melatonin (MEL), Ursodeoxycholic acid (UDCA) and Balanites aegyptiaca (BA) against hepatotoxicity induced by MTX for one month. Methods Eighty adult male rats (Sprague Dawely) weighing (190 ± 10 g), were randomly divided into eight equal groups: Control, MTX, MEL, BA, UDCA, MTX + MEL, MTX + BA, MTX + UDCA. Liver function biomarker enzymes, liver tissue oxidative stress parameters, together with total antioxidant capacity and tumor necrosis factor (TNF-α) were determined. Histopathological and immunohistochemistry examinations for TNF-α were also done. Results MTX showed significant increase in alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), total and direct bilirubin, as well as TNF-α levels, oxidized glutathione (GSSG), malodialdehyde (MDA) and nitric oxide (NO). Whereas total protein, albumin, total antioxidant capacity, reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) levels were significantly decreased in MTX treated group. These alterations were improved by MEL and BA treatment, whereas no improvement was noticed in UDCA treatment. Conclusions BA may be as promising as MEL in the hepatoprotection against MTX toxicity through their antioxidant and radical scavenging activities. In addition, it is not recommended to co-administer UDCA with MTX as it enhanced inflammation and damage to the liver.