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

• Published in: Journal of cellular and molecular medicine Vol. 28; no. 8; pp. e18196 - n/a
• Main Authors: Saad, Hebatallah M., Oda, Samah S., Alexiou, Athanasios, Papadakis, Marios, Mahmoud, Mohamed H., Batiha, Gaber El‐Saber, Khalifa, Eman
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01-04-2024; John Wiley and Sons Inc
• Subjects: Actin; Alanine transaminase; Animals; Anorexia; Aspartate aminotransferase; Biochemical markers; Calcium Carbonate; Caspase-3; Chemical and Drug Induced Liver Injury - pathology; Cirrhosis; Collagen; Collagen - metabolism; Drug Combinations; Fibrosis; Flavonoids - pharmacology; Hepatotoxicity; histopathology; Humans; Inclusion bodies; Inflammation; Ki-67 Antigen - metabolism; Lactose; Lactéol® forte; Leukocytes (eosinophilic); Liver; Liver - metabolism; Liver cirrhosis; Liver Cirrhosis - metabolism; Male; Microbiota; Mortality; Original; Oxidative Stress; Probiotics; Quercetin; Quercetin - pharmacology; quercetin dihydrate; Rats; Smooth muscle; Statistical analysis; Thioacetamide; Thioacetamide - toxicity; γ-Glutamyltransferase; United States > US; Egypt; India; histopathology; Thioacetamide; rats; Lactéol® forte; liver; quercetin dihydrate
• ISSN: 1582-1838; 1582-4934
• DOI: 10.1111/jcmm.18196

Liver 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.