The pharmaceutical Impacts of honeybee venom against thioacetamide-induced hepatic fibrosis in rats

Abstract

Hepatic cirrhosis is an acute disease accompanying fibrosis, liver cell damage, and liver dysfunction. The current study, the prospective therapeutic effects of honey bee venom (BV) on liver fibrosis were examined in rats administered thioacetamide. Hepatic histology, Masson’s trichrome, anti-oxidants (total glutathione and superoxide dismutase), apoptosis and biochemical hepatic functions assays were estimated. We found that BV treatment up-regulated the albumin protein, anti-oxidant enzymes (GSH and SOD) and down-regulated aspartate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, collagen formation and apoptotic rate, which were altered by TAA inducer. Together, these responses increased liver cells sensitivity to TAA-induced hepatotoxicity and forced the damaged cells to undergo apoptosis. Enhancing the tendency of damaged liver cells to undergo apoptosis could be a protective mechanism whereby BV suppresses inflammatory responses and liver fibrosis. The study suggested that honeybee venom prevented TAA-induced liver fibrosis by inhibiting liver inflammation; decreased the high rate of lethality; alleviated hepatic histological injury; attenuated hepatic inflammatory responses; and inhibited hepatic cells apoptosis. These results suggest that honeybee venom could be an effective agent for preventing liver fibrosis.

Keywords: Hepatic fibrosis, Honey bee venom, Thioactamide, Antioxidants