Planta Med 2008; 74 - PA339
DOI: 10.1055/s-0028-1084336

Hepatoprotective effect of Pistacia lenticus var. Chia total extract against carbon tetrachloride-induced liver damage in rats

SK Mavridis 1, O Gortzi 2, S Lalas 2, S Paraschos 3, AL Skaltsounis 3, IS Pappas 1
  • 1Laboratory of Veterinary Pharmacology and Toxicology, Faculty of Veterinary Medicine, University of Thessaly, Trikalon 224, 43100 Karditsa, Greece
  • 2Department of Food Technology, Technological Educational Institution (T.E.I.) of Larissa (Karditsa Annex), Terma N. Temponera str., GR-43100, Karditsa, Greece
  • 3Laboratory of Pharmacognosy & Natural Products Chemistry, Department of Pharmacy, University of Athens, Panepistimiopolis Zografou, GR 15771, Athens, Greece

Reactive oxygen species (ROS) are involved in a number of diseases including cellular aging, mutagenesis, carcinogenesis, coronary heart disease and cardiovascular disorders, diabetes, inflammation, arthritis, dementia and neurodegeneration. In the present study, we investigated whether total extracts from Chios mastic (Pistacia lentiscus var. chia) can protect liver from carbon tetrachloride (CCl4)-induced liver damage in Wistar rats. Mastic gum total extracts (1.5mg/kg), silimarin (SIL) (50mg/kg) were administrated intraperitoneously for 3 consecutive days prior to administration of CCl4 (1.5ml/kg) (ip) to each animal, and 48 hr later the rats were killed by decapitation. Livers were isolated and homogenized. The levels of malondialdehyde (MDA) and glutathione (GSH), and the activity of glutathione related enzymes [glutathione peroxidase (GPx), glutathione S-transferase (GST) and glutathione reducase (GR)], superoxide dismutase (SOD) and catalase (CAT) were then determined. Animals treated with mastic and SIL alone showed a decrease in levels of AST, ALT and MDA either in control or in CCl4-treated rats. These results suggest that mastic gum extracts and SIL have a strong inhibitory effect against lipid peroxidation in rat livers. The CCl4-treated group showed a significantly reduced GSH level but the pre-treatment with mastic gum and SIL inhibited GSH depletion caused by CCl4, yielding GSH levels comparable to that observed in untreated rats. Mastic gum and SIL increased the content of GSH in the rat liver compared to control rats. The CCl4-treated group showed a significantly reduced GSH level but the pre-treatment with mastic gum and SIL greatly reduced GSH depletion. Similar results have been observed in activities of GSH-related enzymes, SOD and CAT. In conclusion, mastic gum total extracts could protect liver cells from CCl4-induced oxidative damage.