Abstract
Background: Nonalcoholic fatty liver disease (NAFLD) is emerging one of the major causes of chronic liver damage that includes a wide spectrum of liver injury ranging from steatosis to steatohepatitis evolving to fibrosis. Aim: This study was designed to evaluate the possible effect of EUG on NAFLD induced by high fat cholesterol diet. Methods:Rats were fed either normal rat chow diet (control) or high fat cholesterol diet and both received olive oil (10 mg/kg) for eight weeks to induce NAFLD model. Eugenol (10 mg/kg) was administrated to rats by oral intubation 3 times weekly for 8 weeks. Results:Our results showed that EUG significantly ameliorated the histopathological lesions induced by HFCD. Furthermore, HFCD induced a significant elevation in liver enzymes (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)). This was significantly attenuated by EUG co-treatment. Conclusion:These findings indicate that EUG possess es a marked role in modulation of NAFLD.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. It represents a spectrum of disease, ranging from simple steatosis to steatohepatitis through to fibrosis and cirrhosis (Than and Newsome, 2015)
Nonalcoholic fatty liver disease (NAFLD) is recognized as the most common form of liver disease worldwide affecting between 25-30% of the general population
As a consequence of excess lipid contents that spill over from the dysfunctional adipose tissue, ectopic lipid deposition in liver would occur (Stienstra et al, 2010). This flux in particular is a major determinant of accumulation of hepatic and lipoprotein fat in NAFLD that induce marked liver injury (Loria et al, 2008)
Summary
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome It represents a spectrum of disease, ranging from simple steatosis to steatohepatitis through to fibrosis and cirrhosis (Than and Newsome, 2015). NAFLD is recognized as the most common form of liver disease worldwide affecting between 25-30% of the general population. As a consequence of excess lipid contents that spill over from the dysfunctional adipose tissue, ectopic lipid deposition in liver would occur (Stienstra et al, 2010). This flux in particular is a major determinant of accumulation of hepatic and lipoprotein fat in NAFLD that induce marked liver injury (Loria et al, 2008). Nonalcoholic fatty liver disease (NAFLD) is emerging one of the major causes of chronic liver damage that includes a wide spectrum of liver injury ranging from steatosis to steatohepatitis evolving to fibrosis
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