It has been shown that phosphatidylcholine (PC) extracted from egg yolk possesses a variety of biological activities, such as anti-inflammatory and anti-oxidant effects, and prevents oxidative stress. The aim of this study was to evaluate the hepatoprotective effects of PC against carbon tetrachloride (CCl₄), which is a well-known hepatotoxicant that causes extensive oxidative liver damage, and to investigate the mechanisms involved in this protective effect. Mice were treated with PC (0.1 ml, 10 or 100 mg/kg, orally) once daily for 5 consecutive days prior to CCl₄ administration (0.1 ml, 20 mg/kg, intraperitoneally). The experimental data show that pretreatment with PC significantly prevented increases of serum aspartate transaminase, alanine transaminase, and alkaline phosphatase, and reduced reactive oxygen species levels. Histopathological evaluation of the liver also revealed that PC effectively ameliorated CCl₄-induced hepatic injury and fibrosis. In addition, PC significantly counteracted the increase in glutathione levels and glutathione-S-transferase activity induced by CCl₄. Concordantly, PC significantly decreased CCl₄-induced upregulation of apoptotic proteins in the liver. These results suggest that PC exerts its protective effects against CCl₄-induced hepatotoxicity via its activities as an anti-oxidant and free radical scavenger.
Keywords: Carbon tetrachloride; Fibrosis; Hepatotoxicity; Oxidative stress; Phosphatidylcholine.
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