title: Caffeine intake decreases oxidative stress and inflammatory biomarkers in experimental liver diseases induced by thioacetamide: Biochemical and histological study.
abstract: Liver disease remains a significant global health problem. Increased caffeine consumption has been associated with a lower prevalence of chronic liver disease. This study aimed to investigate the modifying effects of caffeine on liver injury induced by thioacetamide (TAA) administration in male rats and the possible underlying mechanisms. Forty adult male rats were equally classified into four groups: control group, received only tap water; caffeine-treated group, received caffeine (37.5 mg/kg per day); TAA-treated group, received intraperitoneal (i.p.) TAA (200 mg/kg b.w.) twice a week; and caffeine + TAA-treated group, received combined TAA and caffeine in the same previous doses. After eight weeks of treatment, blood samples were collected for biochemical analysis and liver specimens were prepared for histological and immunohistochemical studies and for assessment of oxidative stress. TAA induced liver toxicity with elevated liver enzymes and histological alterations, fatty changes, apoptosis, and fibrosis evidenced by increased immunohistochemical reaction to matrix metalloproteinase-9 (MMP-9) and collagen type IV in hepatocytes. Also, the levels of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) in serum were significantly elevated. Co-treatment with caffeine and TAA restored normal liver structure and function. Caffeine provided an anti-fibrogenic, anti-inflammatory, and antioxidant effect that was associated with recovery of hepatic histological and functional alterations from TAA-induced hepatotoxicity.
authors.affiliation: 1 Department of Histology & Cell Biology, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
authors.forename: Mona G
authors.initials: MG
authors.lastname: Amer
authors.affiliation: 1 Department of Histology & Cell Biology, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
authors.forename: Nehad F
authors.initials: NF
authors.lastname: Mazen
authors.affiliation: 2 Department of Medical Pharmacology, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
authors.forename: Ahmed M
authors.initials: AM
authors.lastname: Mohamed
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000469:Alkaline Phosphatase / Q000097:blood; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D001219:Aspartate Aminotransferases / Q000097:blood; D001663:Bilirubin / Q000032:analysis; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D002110:Caffeine / Q000494:pharmacology / Q000627:therapeutic use; D056486:Chemical and Drug Induced Liver Injury / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D024141:Collagen Type IV / Q000378:metabolism; D016207:Cytokines / Q000097:blood; D004195:Disease Models, Animal; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D013853:Thioacetamide; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D015415:Biomarkers; D024141:Collagen Type IV; D016207:Cytokines; D013853:Thioacetamide; D002110:Caffeine; D005979:Glutathione Peroxidase; D005723:gamma-Glutamyltransferase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D000469:Alkaline Phosphatase; D020780:Matrix Metalloproteinase 9; C572337:Mmp9 protein, rat; D005978:Glutathione; D001663:Bilirubin
keywords: MMP-9; TNF-α; caffeine; fibrosis; liver