Apilarnil alleviates paracetamol-induced hepatotoxicity by modulating apoptosis and oxidative stress.

Abstract

Paracetamol (PAR) is a drug that is widely used throughout the world and has limited treatment options in case of use-related hepatotoxicity. Apilarnil (AP), a bee product has high levels of antioxidant properties, which result from the rich polyphenols found in its structure. Despite it being shown that AP treatment might have a protective effect on liver damage induced by carbon tetrachloride and lipopolysaccharide, there is no study investigating the possible role of this agent in PAR-induced hepatotoxicity using an experimental in vivo model. Therefore, we aimed to investigate the therapeutic effects of AP on paracetamol-induced hepatotoxicity and its relationship with apoptosis and oxidative stress. Our results indicated that PAR administration caused irregularities in hepatocyte cords, bleeding and dilatation of sinusoids, and inflammatory cell infiltration in the portal area and liver parenchyma. PAR caused an increase in p53 and caspase3 expressions and malondialdehyde (MDA) levels, while it caused a decrease in catalase (CAT) and glutathione peroxidase (GSHpx) levels. AP treatment significantly improved histopathological changes in liver tissues and decreased p53 and caspase3 expressions. Our data suggest that AP alleviates paracetamolinduced hepatotoxicity by regulating p53 and caspase-3 expressions and modulating oxidative stress mechanisms.