A novel cerebroside from lycii fructus preserves the hepatic glutathione redox system in primary cultures of rat hepatocytes.

We previously reported the isolation of a novel cerebroside (1-O-(beta-D-glucopyranosyl)-(2S,3R,4E,8Z)-2-N-palmityloc tadecasphinga-4,8-diene; LCC) from the fruits of Lycium chinense MILL. (Solanaceae) which protected primary cultured rat hepatocytes from the toxicity induced by carbon tetrachloride (CCl4). The present study was conducted to determine the mechanism(s) by which LCC might exert its hepatoprotective activity. To determine the effect of LCC on the glutathione (GSH) redox system, we measured the activities of enzymes involved in the system as well as the levels of hepatic mitochondrial GSH and malondialdehyde (MDA). The hepatotoxicant, CCl4, routinely decreased levels of total and reduced GSH. The levels of these compounds were significantly maintained at the levels of the control cultures following treatment with LCC. The decreased activities of glutathione reductase and glutathione peroxidase in CCl4-injured rat hepatocytes were significantly increased by the treatment of LCC. Furthermore, the elevated levels of MDA seen in CCl4-injured rat hepatocytes were reduced after treatment with LCC in a concentration dependent manner over a range of 1-10 microM. From these results, we postulate that LCC may preserve the hepatic mitochondrial level of GSH by scavenging reactive oxygen species produced during CCl4-induced toxicity and thereby reduce lipid peroxidation and cellular damage.