Ameliorating effects of Myrcene, a monoterpene in many plants, on thioacetamide-induced acute hepatic encephalopathy in rats

Hepatic encephalopathy (HE) is a clinical syndrome which can observe because of acute and chronic liver disorders such as hepatitis, liver failure caused by alcohol or drugs, autoimmune diseases, metabolic diseases, cirrhosis, types of tumors and infections. We aimed to investigate the effects of different doses of β-myrcene on the improvement of hepatic encephalopathy caused by thioacetamide (TAC) in male rats. In order to induce liver failure and acute damage in the studied animals, thioacetamide was administered to rats with a dose 100 mg/kg of body weight as an intraperitoneal (IP) injection with 24 h intervals and for seven consecutive days. After oral treatment of rats with β-myrcene at doses of 10, 25, and 50 mg/kg/day for 7 days, the cerebral edema (brain water content, BWC), the serum level of aspartate aminotransferase (AST), alanine transferase (ALT) and alkaline transferase (ALP), total protein (TP), bilirubin (TB), and ammonia as well as the level oxidant-antioxidant factors of malondialdehyde (MDA), glutathione peroxidase (GPx), Catalase (CAT) and superoxide dismutase enzymes (SOD) were evaluated. β-myrcene dose dependently reduced the BWC in Thioacetamide-induced acute hepatic encephalopathy in rats. Treatment of the TAC rats with β-myrcene especially at doses of 25 and 50 mg/kg significantly (p<0.001) moderated the serum level of these liver enzymes and ammonia compared to the untreated TAC mice. The analysis of the obtained data revealed that the treatment of the TAC rats with β-myrcene especially at doses of 25 and 50 mg/kg markedly (p<0.001) reduced the oxidative stress of MDA, whereas significantly (p<0.001) increased antioxidant enzymes of SOD, CAT, and GPx. Therefore, we can conclude that the treatment of the TAC rats with β-myrcene especially at doses of 25 and 50 mg/kg markedly reduced the oxidative stress of MDA, whereas significantly increased antioxidant enzymes and subsequently improved the thioacetamide-induced acute hepatic encephalopathy in rats.