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The Effects of 10 Triterpenoid Compounds on Experimental Liver Injury in Mice
Authors:LIU  LIE; LIU  YAPING; MAO  QING; KLAASSEN  CURTIS
Institution: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

Abstract:The purpose of this study was to compare the hepatoprotec tiveeffects of 10 oleanane-type triterpenoid compounds on threeknown hepatotoxicants in mice. These compounds in clude oleanolicacid, 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 wereadministrated sc for 3 days at 200 µmol/kg, except for{alpha}-H, which was given at 100 , imol/kg for 2 days. Acute liverinjury was produced in male CF-1 mice by CCI (15 µl/kg,ip), acetaminophen (500 mg/kg, ip), and cadmium chloride (3.7mg/kg, iv). Liver damage was assessed by serum activities ofalanine aminotransferase and sorbitol dehydrogenase, as wellas by his topathological examination. {alpha}-Hedenn, ursolic acid,and olean olic acid markedly decreased the toxicity producedby all three hepatotoxicants. Uvaol significantly decreasedCd and Cd- induced hepatotoxicity, but had no effect on acetaminophentox icity. Glycyrrhizin, {alpha}-GA, and ß-GA decreased acetaminopheninduced liver injury, whereas hederagenin, HAG, and HA did notprotect against any of the hepatotoxicants. In addition, {alpha}-hederin,ursolic acid, oleanolic acid, and uvaol increased hepatic metallothioneinlevels by 87-, 48-, 28-, and 1 0-fold, respectively, as determinedby the Cd/hemoglobin assay. In conclusion, among the 10 triterpenoidcompounds examined, {alpha}-hederin, ur solic acid, and oleanolic acidappear to be the most effective in protecting against CCl4-acetaminophen-, and Cd-induced liver injury.
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