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© 1994 Oxford University Press

research-article

The Effects of 10 Triterpenoid Compounds on Experimental Liver Injury in Mice1

LIE LIU, YAPING LIU, QING MAO* and CURTIS KLAASSEN

Department of Pharmacology, Toxicology and Therapeutics, Environmental Health and Occupational Medicine Center, University of Kansas Medical Center, Kansas City Kansas 66160-7417 *Guizhou Traditional Medical Institute Guiyang China

Received February 10, 1993; accepted September 2, 1993

The purpose of this study was to compare the hepatoprotec tive effects of 10 oleanane-type triterpenoid compounds on three known hepatotoxicants in mice. These compounds in clude oleanolic acid, ursolic acid, uvaol, {alpha}-hederin ({alpha}-H), heder agenin, glycyrrhizin, 18{alpha}-glycyrrhetinic acid ({alpha}-GA), 18ß-glycyrrhetinic acid (ß-GA), 19{alpha}-hydroxyl asiatic acid 28-O-ß-D- glucoside (HAG), and 19{alpha}-hydroxyl asiatic acid (HA). They were administrated sc for 3 days at 200 µmol/kg, except for {alpha}-H, which was given at 100 , imol/kg for 2 days. Acute liver injury was produced in male CF-1 mice by CCI (15 µl/kg, ip), acetaminophen (500 mg/kg, ip), and cadmium chloride (3.7 mg/kg, iv). Liver damage was assessed by serum activities of alanine aminotransferase and sorbitol dehydrogenase, as well as by his topathological examination. {alpha}-Hedenn, ursolic acid, and olean olic acid markedly decreased the toxicity produced by all three hepatotoxicants. Uvaol significantly decreased Cd and Cd- induced hepatotoxicity, but had no effect on acetaminophen tox icity. Glycyrrhizin, {alpha}-GA, and ß-GA decreased acetaminophen induced liver injury, whereas hederagenin, HAG, and HA did not protect against any of the hepatotoxicants. In addition, {alpha}-hederin, ursolic acid, oleanolic acid, and uvaol increased hepatic metallothionein levels by 87-, 48-, 28-, and 1 0-fold, respectively, as determined by the Cd/hemoglobin assay. In conclusion, among the 10 triterpenoid compounds examined, {alpha}-hederin, ur solic acid, and oleanolic acid appear to be the most effective in protecting against CCl4- acetaminophen-, and Cd-induced liver injury.


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