Hepatoprotective activity of Lactéol® forte and quercetin dihydrate against thioacetamide‐induced hepatic cirrhosis in male albino rats

Author:

Saad Hebatallah M.1ORCID,Oda Samah S.2,Alexiou Athanasios3456ORCID,Papadakis Marios7,Mahmoud Mohamed H.8,Batiha Gaber El‐Saber9,Khalifa Eman10

Affiliation:

1. Department of Pathology, Faculty of Veterinary Medicine Matrouh University Matrouh Egypt

2. Department of Pathology, Faculty of Veterinary Medicine Alexandria University Abees Alexandria Province Egypt

3. University Centre for Research & Development Chandigarh University Mohali Punjab India

4. Department of Research & Development Funogen Athens Greece

5. Department of Research & Development AFNP Med Wien Austria

6. Department of Science and Engineering Novel Global Community Educational Foundation Hebersham New South Wales Germany

7. Department of Surgery II University Hospital Witten‐Herdecke, Heusnerstrasse 40, University of Witten‐Herdecke Wuppertal Germany

8. Department of Biochemistry, College of Science King Saud University Riyadh Kingdom of Saudi Arabia

9. Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine Damanhour University Damanhour AlBeheira Egypt

10. Department of Microbiology, Faculty of Veterinary Medicine Matrouh University Matrouh Egypt

Abstract

AbstractLiver cirrhosis is a silent disease in humans and is experimentally induced by many drugs and toxins as thioacetamide (TAA) in particular, which is the typical model for experimental induction of hepatic fibrosis. Thus, the objective of the present study was to elucidate the possible protective effects of lactéol® forte (LF) and quercetin dihydrate (QD) against TAA‐induced hepatic damage in male albino rats. Induction of hepatotoxicity was performed by TAA injection (200 mg/kg I/P, twice/ week) in rats. LF (1 × 109 CFU/rat 5 times/week) and QD (50 mg/kg 5 times/week) treated groups were administered concurrently with TAA injection (200 mg/kg I/P, twice/ week). The experimental treatments were conducted for 12 weeks. Hepatotoxicity was evaluated biochemically by measuring alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma‐glutamyl transferase (GGT) in the serum and histopathologically with the scoring of histopathological changes besides histochemical assessment of collagen by Masson's trichrome and immunohistochemical analysis for α‐smooth muscle actin (α‐SMA), Ki67 and caspase‐3 expression in liver sections. Our results indicated that LF and QD attenuated some biochemical changes and histochemical markers in TAA‐mediated hepatotoxicity in rats by amelioration of biochemical markers and collagen, α‐SMA, Ki67 and caspase3 Immunoexpression. Additionally, LF and QD supplementation downregulated the proliferative, necrotic, fibroblastic changes, eosinophilic intranuclear inclusions, hyaline globules and Mallory‐like bodies that were detected histopathologically in the TAA group. In conclusion, LF showed better hepatic protection than QD against TAA‐induced hepatotoxicity in rats by inhibiting inflammatory reactions with the improvement of some serum hepatic transaminases, histopathological picture and immunohistochemical markers.

Publisher

Wiley

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