Abstract
The mechanism of antihepatotoxic action of atractylon, a main sesquiterpenic constituent of Atractylodes rhizomes, was studied. Atractylon inhibited carbon tetrachloride (CCl4)-induced cytotoxicity in primary cultured rat hepatocytes and CCl4-induced lipid peroxidation by rat liver microsomes. However, atractylon increased the free radical generation by CCl4 with rat liver microsomes in the presence of a radical trapping agent, phenyl t-butyl nitrone (PBN). In addition, atractylon generated free radical per se. Experiments using 13CCl4 instead of CCl4 indicated that the increased free radicals consisted of those from 13CCl4 and from atractylon. Accumulated data support that although both CCl4 and atractylon generate free radicals respectively by rat liver microsomes, free radical from CCl4 conducts lipid peroxidation and produces liver lesion, while atractylon forms free radical which scavenges CCl3 radical in the absence of PBN, inhibits lipid peroxidation by CCl4 and suppresses CCl4-induced liver lesion.
Published Version
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