Trianthema portulacastrum L. reverses hepatic lipid peroxidation, glutathione status and activities of related antioxidant enzymes in carbon tetrachloride-induced chronic liver damage in mice.

To understand the mechanism of the antihepatotoxic potential of an ethanolic extract of Trianthema portulacastrum, experiments were carried out to monitor its effect on hepatic lipid peroxidation, glutathione status and activities of several antioxidant enzymes following the chronic treatment of mice with carbon tetrachloride (CCl(4)). CCl(4) was administered orally three times a week for five weeks. Daily oral treatment with the extract (100 or 150 mg/kg) was started two weeks prior to the commencement of CCl(4) administration and continued for a total seven consecutive weeks. The significantly elevated lipid peroxidation of the liver due to chronic CCl(4) treatment was reduced towards normalization in a dose-dependent manner following the treatment with the extract. When compared to the control animals, the CCl(4)-treated mice showed both significant decrease in their hepatic-reduced glutathione (GSH) level and an increase in their oxidized glutathione (GSSG) level; meanwhile their GSH/GSSG ratio experienced corresponding fall. The extract therapy restored these altered features near normalcy in a dose-responsive manner. The extract also produced dose-dependent increase in the activity of glutathione reductase and a decrease in catalase, glutathione peroxidase and glutathione S-transferase in the liver. Those were otherwise substantially reversed by CCl(4) treatment alone. The results of our investigation strongly indicate that the hepatoprotective activity of T. portulacastrum is mediated through a marked inhibition of toxicant-induced hepatic lipid peroxidation with a concurrent modulation of GSH status and the activities of antioxidant defense enzymes in mouse liver.