Ameliorating Effects of β-Myrcene, a Monoterpene in Many Plants, on Thioacetamide-Induced Acute Hepatic Encephalopathy in Rats.

Abstract

Hepatic encephalopathy (HE) is a clinical syndrome that can result from acute and chronic liver disorders, such as hepatitis, liver failure caused by alcohol or drugs, autoimmune diseases, metabolic diseases, cirrhosis, different types of tumors, and infections. This study aimed to investigate the effects of different doses of Beta-myrcene (β-myrcene) on the improvement of HE caused by thioacetamide (TAC) in male rats. To induce liver failure and acute damage in the studied animals, TAC was administered to rats at a dose of 100 mg/kg of body weight through an intraperitoneal (IP) injection with 24-hour intervals for seven consecutive days. After the oral treatment of rats with β-myrcene at doses of 10, 25, and 50 mg/kg/day for seven days, the cerebral edema (brain water content, BWC), the serum level of liver enzymes (aspartate aminotransferase, alanine transferase, alkaline transferase, total protein, and bilirubin), ammonia, and the level of oxidant-antioxidant factors (lipid peroxidation [MDA], glutathione peroxidase [GPx], catalase [CAT], and superoxide dismutase enzymes [SOD]), were evaluated. β-myrcene dose-dependently reduced BWC in TAC-induced acute HE in rats. In TAC rats treated with β-myrcene, especially at doses of 25 and 50 mg/kg, the serum levels of these liver enzymes and ammonia were significantly moderated (P<0.001), compared to the untreated TAC rats. The analysis of the obtained results revealed that the treatment of TAC rats with β-myrcene, especially at doses of 25 and 50 mg/kg, significantly reduced the oxidative stress marker MDA (P<0.001), whereas it significantly increased the antioxidant enzymes SOD, CAT, and GPx (P<0.001). Therefore, it can be concluded that the treatment of TAC rats with β-myrcene, especially at doses of 25 and 50 mg/kg, significantly reduced the oxidative stress marker MDA, whereas it significantly increased antioxidant enzymes and subsequently improved TAC-induced acute HE in rats.