Abstract

Primary cultures of rat hepatocytes exposed to galactosamine (GalN) were used as a screening system to assess whether a new cerebroside, LCC, isolated from the fruits of Lycium chinense, exhibits hepatoprotective activity. Cultured rat hepatocytes injured with GalN routinely release glutamic pyruvic transaminase (GPT) and sorbitol dehydrogenase (SDH) into the culture medium. Treatment of these GalN-injured primary cultures with LCC markedly blocked the release of both GPT and SDH in a dose-dependent manner over concentrations of LCC ranging from 1 microM to 10 microM. To investigate the mechanism of action for the hepatoprotective activity of LCC, the extent of [(3)H]-uridine incorporation into RNA was measured in GalN-injured cultures of rat hepatocytes. [(3)H]-Uridine incorporation was significantly decreased in injured hepatocytes. LCC, however significantly restored the incorporation of [(3)H]-uridine into RNA in a dose-dependent manner over concentrations ranging from 1 microM to 10 microM. LCC also blocked the suppression of RNA synthesis caused by actinomycin D in a dose-dependent manner. These data suggest that LCC may have prominent hepatoprotective activity and that its therapeutic value should be investigated further.

Copyright 2000 John Wiley & Sons, Ltd.