Unsweetened Theobroma cacao powder mitigates oxidative stress and preserves hepatic function in ethanol-fed Sprague Dawley rats

Theobroma cacao and hepatic oxidative stress

  • Ernest Amponsah Asiamah University of Cape Coast
  • Angelina A Ampah Department of Biomedical Sciences, School of Allied Health Sciences, University of Cape Coast, Cape Coast, Ghana
  • Francis Tambo Department of Forensic Sciences, School of Biological Sciences, University of Cape Coast, Cape Coast, Ghana
  • Moses Adjei Department of Biomedical Sciences, School of Allied Health Sciences, University of Cape Coast, Cape Coast, Ghana
  • Jude Forson Department of Biomedical Sciences, School of Allied Health Sciences, University of Cape Coast, Cape Coast, Ghana
  • Belinda S Amoakoa Department of Biomedical Sciences, School of Allied Health Sciences, University of Cape Coast, Cape Coast, Ghana
  • Andrews F Wiafe Department of Biomedical Sciences, School of Allied Health Sciences, University of Cape Coast, Cape Coast, Ghana
  • Jake B Adom-Yeboah Department of Biomedical Sciences, School of Allied Health Sciences, University of Cape Coast, Cape Coast, Ghana
  • Denzel OPOKU-KWABI Opoku-Kwabi Department of Biomedical Sciences, School of Allied Health Sciences, University of Cape Coast, Cape Coast, Ghana
  • Benjamin Aboagye Department of Forensic Sciences, School of Biological Sciences, University of Cape Coast, Cape Coast, Ghana
DOI: https://doi.org/10.46829/hsijournal.2026.4.8.2.1456-1467
Keywords: Theobroma cacao, oxidative stress, ethanol, liver

Abstract

Background: Morphological evidence suggests that unsweetened cocoa powder (UCP) prevents hepatic injury in experimental ethanol ingesting animal models, possibly due to its antioxidant and anti inflammatory potentials. However, the functional integrity of hepatocytes and the underlying mechanisms are underexplored.
Objective: This study investigated the protective effect of UCP on liver function in ethanol-ingesting male Sprague-Dawley rats.
Methods: Male rats (200-220 g) were fed daily for 8 weeks with either 30% ethanol, 300 mg/kg UCP p.o, or 30% ethanol and 300 mg/kg UCP p.o. 6 h later. Rats that were neither fed with UCP nor ethanol served as controls. At the experimental endpoint, cardiac blood was collected for liver function test, prothrombin time and C-reactive protein assay. The large lobe of the liver was processed and stained with periodic acid Schiff (PAS) and lipofuschin. PAS-stained livers were used for hepatocyte glycogen estimation. The remaining lobes were homogenised for total antioxidant capacity and catalase activity assays.
Results: Compared to the control, ethanol-only-fed rats showed lower serum total protein, albumin, and globulin, and lower hepatocyte glycogen, and higher prothrombin time. Also, ethanol-only-fed rats showed increased serum AST/ALT ratio, CRP, total bilirubin, and unconjugated bilirubin, but reduced conjugated bilirubin. Additionally, the livers of the ethanol-only-fed rats exhibited increased TAC, low catalase and increased lipofuscin accumulation. However, compared with ethanol-only-fed rats, UCP-treated ethanol-fed rats showed higher serum total protein, albumin, and globulin, and higher hepatocyte glycogen, and a lower prothrombin time. UCP-treated ethanol-fed rats also exhibited higher serum conjugated bilirubin, lower unconjugated bilirubin, less lipofuscin accumulation, and higher TAC and catalase levels compared to the ethanol-only-fed rats.
Conclusion: Ingestion of UCP alongside ethanol not only attenuates hepatocellular damage but also preserves hepatic function, possibly by mitigating inflammation and oxidative stress. Thus, UCP could protect against alcohol-induced liver damage. 

Published
2026-03-30
Issue
Vol 8 No 2 (2026): Health Sciences Investigations (HSI)  Journal
Section
Original Research Article