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Updated: May 20, 2026
The Murine Choline-Deficient, Ethionine-Supplemented (CDE) Diet Model of Chronic Liver Injury
Published on: October 21, 2017
Hepatoprotective effects of cinnamaldehyde against high-fat diet-induced liver damage
Reyhane Farmani1, Mehran Hosseini2, Samaneh Nakhaee3
1Student Research Committee, Birjand University of Medical Sciences, Birjand, Iran.
Objective:
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder worldwide, affecting 30-40% of adults. High-fat diets contribute significantly to NAFLD by promoting hepatic lipid accumulation, oxidative stress, and inflammation. In this context, cinnamaldehyde (CNMA) has emerged as a promising hepatoprotective agent due to its antioxidant, anti-inflammatory, and lipid-regulatory properties.
Materials And Methods:
Male Wistar rats were randomly assigned to four groups (n=6 per group): (A) Control; (B) HFD; (C) Control+CNMA; and (D) HFD+CNMA. CNMA was administered orally at 20 mg/kg body weight for 16 weeks simultaneously with HFD. At the end of the study, rats were fasted for 12-14 hr and anesthetized with sodium pentobarbital (60 mg/kg, intraperitoneal) for serum, liver, and visceral adipose tissues collection. Biochemical analyses included serum liver enzymes, lipid profiles, hepatic triglyceride levels, and oxidative stress markers (nitric oxide metabolites; NOx, and malondialdehyde; MDA). Histopathological evaluation was performed on H&E (Hematoxylin and Eosin)-stained liver sections.
Results:
HFD feeding induced significant hepatic injury and metabolic dysfunction in rats, characterized by elevated AST (Aspartate aminotransferase) and ALT (Alanine aminotransferase) levels, increased liver and fat pad weights, and enhanced oxidative stress. CNMA treatment significantly reduced these parameters, resulting in lower serum liver enzymes, decreased hepatic triglyceride content, reduced adiposity (notably mesenteric fat), and ameliorated oxidative stress. Histopathological findings confirmed a reduction in micro- and macrovesicular steatosis with CNMA.
Conclusion:
CNMA significantly protected against HFD-induced hepatic injury by reducing serum AST and ALT, hepatic triglycerides, visceral adiposity, and oxidative stress and inflammatory markers, as confirmed by histopathology. It suggests the therapeutic potential of CNMA for NAFLD and related metabolic disorders.
