Abstract
Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of liver diseases that occur in individuals who do not consume a significant amount of alcohol, and the pathogenesis of NAFLD remains undefined. It was aimed to investigate whether the use of Trimetazidine (TMZ) could reduce warm ischemia-reperfusion (I/R) damage after liver ischemia on an experimental NAFLD model in this experimental study. Methods: For this aim, Sprague Dawley male rats were separated into 4 groups; control group (group 1, n = 6), sham operated control grup (group 2, n = 6), warm ischemia/reperfusion group (group 3, n=10), and TMZ group (group 4, n=10, administration of TMZ (10 mg/kg) 30-min before fatty liver I/R). The serum oxidant and antioxidant biochemical markers were measured by ELISA methods. The histopathological evaluation was also performed in the hepatocytes. Results: TMZ was caused to significantly decrease on oxidative stress markers levels which characterized myeloperoxidase (MPO) (p<0.001), nicotinamide adenine dinucleotide phosphate-oxidase (NOX) (p<0.001), and cytochrome C (Cyt-C) (p<0.001), and increase on antioxidant enzyme catalase (CAT) (p<0.001) activity as compared to group 3. However, TMZ was no caused to any significant change in other oxidant markers malondialdehyde (MDA) and 8-hydroxyguanosine (8-OHDG) levels (p> 0.05). While hepatocyte damage as a form of cell groups was observed due to I/R damage, whereas TMZ had caused positive improvements on dilatation of sinusoids, inflammation and the structural integrity of hepatic plaques. Conclusion: Trimetazidine could be positively contributing effects to the antioxidant defense mechanism and also the survival of cells by protecting mitochondrial integrity.
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