Romanian Society of Pharmaceutical Sciences

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HEME-OXYGENASE-1 UPREGULATED BY S-ADENOSYLMETHIONINE. POTENTIAL PROTECTION AGAINST NON-ALCOHOLIC FATTY LIVER INDUCED BY HIGH FRUCTOSE DIET

GANKA BEKYAROVA1*, MARIA TZANEVA2, KAMELIA BRATOEVA1, ISCREN KOTZEV3, MARIA RADANOVA4

1.Department of Physiology and Pathophysiology, Medical University – Varna, Bulgaria
2.Department of General and Clinical Pathology, Medical University – Varna, Bulgaria
3.Clinic of Gastroenterology MHAT “ST Marina“, Medical University – Varna, Bulgaria
4.Department of Biochemistry, Molecular Medicine and Nutrigenomics, Medical University – Varna, Bulgaria

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Excessive dietary fructose intake may have an important role in the current epidemics of fatty liver disease, obesity and diabetes- features of metabolic syndrome. We evaluated the relationship between lipid peroxidation and other oxidative stress biomarkers with changes in expression of heme oxygenase-1 (HO-1) in rat fatty liver, induced by high fructose diet (HFD) and the effect of S-adenosylmethionine (SAMe). Twenty-one male rats were randomly assigned to three groups of seven animals each: HFD (35% fructose in drinking water for 16 weeks) group, HFD + SAMe (20 mg/kg b.w. in drinking water for 16 weeks) group and control group. HO-1 expression, malonyl dialdehyde (MDA) (a marker of lipid peroxidation), triglycerides (TG), SH group levels and histological studies were performed on hepatic tissue. HFD group showed microvesicular steatosis without inflammation and fibrosis. In HFD+SAM group microvesicular steatosis was not established. The HO-1 expression was significantly increased in HFD rats. SEMe augmented the increase in expression of HO-1. The levels of MDA and TG were elevated in HFD group. In HFD rats with lower levels of SH exhibited higher expression of HO-1. SAMe inhibited the increase in lipid peroxidation and TG levels and prevented the decrease in SH levels. In conclusion, SAMe has an important hepatoprotective effect and its protection is most probably exerted by increasing the expression of the antioxidant enzyme HO-1, in order to prevent the development of fatty liver.