This study was carried out to investigate the protective effects of curcumin on acute or subacute carbon tetrachloride-induced liver damage in rats. Acute hepatotoxicity was induced by intraperitoneal injection of carbon tetrachloride after 4 consecutive days of curcumin treatment. Subacute hepatotoxicity was induced by oral administration of carbon tetrachloride twice a week during 4 weeks of curcumin treatment. In rats with acute liver injury, curcumin (100 and 200 mg kg(-1)) lowered the activity of serum alanine aminotransferase to 52-53% (P < 0.05) and aspartate aminotransferase to about 62% (P < 0.05) those of control rats. In rats with subacute liver injury, curcumin (100 mg kg(-1)) lowered the activity of serum alanine aminotransferase to 34% (P < 0.01) and alkaline phosphatase to 53% (P < 0.05) of control rats. The liver hydroxyproline content in the curcumin (100 mg kg(-1))-treated group was reduced to 48% of the carbon tetrachloride control group (P < 0.01). Malondialdehyde levels in curcumin (100 mg kg(-1)) treated rat liver was decreased to 67% of the control rat liver (P < 0.01) in subacute injury. It was concluded that curcumin improved both acute and subacute liver injury induced by carbon tetrachloride in rats.

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The absorption, dose-linearity and pharmacokinetics of compound K, a major intestinal bacterial metabolite of ginsenosides, were evaluated in vitro and in vivo. Using the Caco-2 cell monolayers, compound K showed moderate permeability with no directional effects, thus suggesting passive diffusion. After intravenous dose (i.v.; 1, 2, and 10 mg/kg), no significant dose-dependency was found in Cl (17.3-31.3 ml/min/kg), Vss (1677-2744 ml/kg), dose-normalized AUC (41.8-57.8 microg.min/ml based on 1 mg/kg) and t1/2. The extent of urinary excretion was minimal for both i.v. and oral doses. The extent of compound K recovered from the entire gastrointestinal tract at 24h were 24.4%-26.2% for i.v. doses and 54.3%-81.7% for oral doses. Following oral administration (doses 5-20 mg/kg), dose-normalized AUC (based on 5 mg/kg) was increased at the 20 mg/kg dose (85.3 microg.min/ml) compared with those at lower doses (4.50-10.5 microg.min/ml). Subsequently, the absolute oral bioavailability (F) was increased from 1.8%-4.3% at the lower doses to 35.0% at the 20 mg/kg dose. The increased F could be related to the saturation of carrier-mediated hepatic uptake and esterification of compound K with fatty acids in the liver.

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