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

Abstract:

: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.

journal_name

Biol Pharm Bull

authors

Kim SY,Lee EJ,Kim HP,Kim YC,Moon A,Kim YC

doi

10.1248/bpb.22.873

subject

Has Abstract

pub_date

1999-08-01 00:00:00

pages

873-5

issue

8

eissn

0918-6158

issn

1347-5215

journal_volume

22

pub_type

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