A comparison of antihepatotoxic activities between glycyrrhizin (18 beta-GL) and its genuine aglycone, glycyrrhetinic acid (18 beta-GA), was carried out using in vivo and in vitro assay methods. The oral administration of 18 beta-GA at 1, 24, and 48 h before D-galactosamine (GalN) treatment significantly reduced the increase of serum transaminase activities 24 h after GalN treatment, whereas 18 beta-GL did not inhibit the increase of serum transaminase activities. The intraperitoneal administration of 18 beta-GA 1 h before GalN treatment restored the increase of serum transaminase activities with lower doses than 18 beta-GL. In CCl4-induced cytotoxicity of primary cultured rat hepatocytes, 18 beta-GA protected the CCl4-induced leakage of transaminase at doses of 5 to 50 micrograms/ml, whereas 18 beta-GL inhibited slightly the leakage at a dose of 1000 micrograms/ml. In the same way, 18 alpha-GA, the alpha-isomer of 18 beta-GA, reduced the CCl4-induced cytotoxicity more strongly than 18 alpha-GL. Furthermore, the adsorbability of 18 alpha, beta-GA on primary cultured rat hepatocytes was higher than that of 18 alpha, beta-GL. These results suggest that 18 alpha, beta-GA is a more potent antihepatotoxic agent than 18 alpha, beta-GL, and that the potency of the antihepatotoxic compounds parallels their adsorbability in hepatocytes.
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