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Non-Alcoholic Fatty Liver Disease (NAFLD) is hepatic manifestation of metabolic syndrome. It represents a spectrum of diseases ranging from steatosis, non-alcoholic steatohepatitis (NASH), that may progress to fibrosis, cirrhosis and eventually hepatocellular carcinoma. Aim: The aim of the study was to investigate the influence of CB1 cannabinoid receptor blockade on the intensity of oxidative/nitrosative stress in mice liver with NAFLD. Therefore, we used rimonabant, selective CB1 antagonist. Material and Methods: Male mice C57BL/6 (n = 28) were divided into following groups: 1) Control group fed with control chow diet 20 weeks (C group; n = 7), 2) Group fed with high saturated fat diet 20 weeks (HF group; n = 7), 3) Group fed with standard chow diet and treated with rimonabant after 18 weeks (R group; n = 7), 4) Group fed with high saturated fat diet and treated with rimonabant after 18 weeks (HFR group; n = 7). The activity of liver transaminases was measured in serum. The concentrations of malondialdehyde (MDA), nitrites and nitrates (NOx), and the activity of superoxide dismutase (SOD), copper/zinc superoxide dismutase (Cu/ZnSOD) and manganese superoxide dismutase (MnSOD) were measured in the liver. Results: Rimonabant induced decrease in transaminase activity in R group compared to control, as well as in HFR group compared to HF group (p < 0.01, respectively). Concentrations of MDA and NOx were lower in HFR compared to HF group (p < 0.01). We found decrease in SOD, Cu/ZnSOD and MnSOD activities in HFR group compared to HF group (p < 0.01). Conclusion: According to the results of this study, it can be concluded that blockade of CB1 receptors causes useful effects in the treatment of NAFLD. Rimonabant reduced hepatocellular injury, which was proved by decreased transaminase activities. The reduction of oxidative/ nitrosative stress and lipid peroxidation may also contribute to the protective effects of rimonabant, which has been shown as decrease in MDA and NOx concentration.

The role of cannabinoid receptor 1 in the development of oxidative/nitrosative stress in mice with non-alcoholic fatty liver disease