Protective effects of apigenin, apigenin-8-sulfonate, and apigenin-3′, 8-disulfonate on d-galactosamine-induced acute liver damage in mice

Abstract

The water-soluble sulfated derivatives, apigenin-8-sulfonate sodium (AS) and apigenin-3′, 8-disulfonate sodium (ADS) derived from parent apigenin (AP), were synthesized and characterized by infrared (IR) spectra, hydrogen nuclear magnetic resonance (1H NMR), carbon nuclear magnetic resonance (13C NMR), high-resolution mass spectra (HRMS), and elemental analysis. The mice model of hepatotoxicity induced by d-Galactosamine (d-GalN) was used to evaluate the hepatoprotective effects of AP, AS, and ADS. The results indicated that AP, AS, and ADS could reduce the level of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and hepatic malondialdehyde (MDA) induced by d-GalN, and restore the activities of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) toward normal levels. The histological results also suggested that AP, AS, and ADS could alleviate liver toxicity. The possible mechanisms could be ascribed to the protection role of AP, AS, and ADS, which kept hepatic cells from oxidative damage and maintain intracellular antioxidant enzyme activity. These findings uncovered that AP, AS, and ADS were able to protect liver from d-GalN-induced acute damage, and AS was the most potent hepatoprotective drug among the three compounds.