Hepatoprotective Effect of Raspberry Ketone Against Carbon Tetrachloride-Induced Rat Hepatic Injury

Abstract

Raspberry ketone (RK) is a natural phenolic compound. The aim of this study was to evaluate the therapeutic detoxification of RK against carbon tetrachloride (CCl4)-induced acute liver injury in vivo and to explore the underlying mechanism, including whether RK regulates inflammation and apoptosis. In this study, seven groups of rats were used: I, Control; II, received 200mg/kg RK for 5 days (PO); III, received a single dose of CCl4diluted with olive oil (1:1 v/v; 1 mL/kg body weight) intraperitoneally on the fifth day; IV, V, VI, and VII received 25, 50, 100, and 200mg/kg RK (PO) daily for 5 days, respectively, with a CCl4intraperitoneal injection on the fifth day. Histopathology, ultra-microstructural examination via transmission electron microscopy, immunohistochemical detection of NF-κB and cytochrome c, DNA fragmentation, and the levels of malondialdehyde, glutathione, tumor necrosis factor-α, and caspase-9 were detected in the liver. Serum liver transaminases were also measured. CCl4induced a significant elevation of serum liver transaminases, as well as increased hepatic malondialdehyde, tumor necrosis factor-α, and caspase-9. In addition, CCl4 increased NF-κB activation, cytochrome c expression, and DNA fragmentation. However, CCl4 decreased hepatic glutathione content. RK pre-treatment significantly ameliorated CCl4 hepatotoxicity, with the highest dose nearly normalizing all measured parameters. In conclusion, RK is a promising protective agent against CCl4 hepatotoxicity, possibly through antioxidant, anti-inflammatory, and anti-apoptotic activities