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.

中文翻译：

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芹菜素，芹菜素-8-磺酸盐和芹菜素-3'，8-二磺酸盐对d-半乳糖胺诱导的小鼠急性肝损伤的保护作用

合成了衍生自亲本芹菜素（AP）的水溶性硫酸化衍生物芹菜素8-磺酸钠（AS）和芹菜素3'，8-二磺酸钠（ADS），并通过红外（IR）光谱，氢核磁共振（¹ H NMR），碳核磁共振（¹³ C NMR），高分辨率质谱（HRMS）和元素分析。d-半乳糖胺（d- GalN）诱导的小鼠肝毒性模型用于评估AP，AS和ADS的肝保护作用。结果表明，AP，AS和ADS可以降低d诱导的血清丙氨酸氨基转移酶（ALT），天冬氨酸氨基转移酶（AST）和肝丙二醛（MDA）的水平。-GalN，并将抗氧化酶超氧化物歧化酶（SOD），谷胱甘肽过氧化物酶（GSH-Px）和过氧化氢酶（CAT）的活性恢复到正常水平。组织学结果还表明，AP，AS和ADS可以减轻肝脏毒性。可能的机制可能归因于AP，AS和ADS的保护作用，它们使肝细胞免受氧化损伤并保持细胞内抗氧化酶活性。这些发现揭示了AP，AS和ADS能够保护肝脏免受d -GalN诱导的急性损伤，并且AS是这三种化合物中最有效的保肝药物。