Traditional drugs or therapies rarely have effects on regression of chronic liver diseases, which result in many cases from sustained oxidative stress. In recent years, ellagic acid (EA) has gained attention due to its multiple biological activities and several molecular targets. This is the first review focused on the pharmacological properties and on the molecular mechanisms activated by EA in terms of liver protection. EA possesses antioxidant, antihepatotoxic, antisteatosic, anticholestatic, antifibrogenic, antihepatocarcinogenic and antiviral properties that improves the hepatic architectural and functions against toxic and pathological conditions. The molecular mechanisms that EA activates include the scavenging of free radicals, regulation of phase I and II enzymes, modulation of proinflammatory and profibrotic cytokines synthesis, the regulation of biochemical pathways involved in the synthesis and degradation of lipids as well as the maintenance of essential trace elements levels. EA also inhibits hepatic stellate cells and mast cells activation, the proliferation of transformed cells, as well as viral replication by increasing antioxidant response, induction of apoptosis, downregulation of genes involved in cell cycle and angiogenesis, and stimulation of cellular immune response. Despite the enormous therapeutic potential of EA as an innovative pharmacological strategy, the number of phase I and II trials in patients is scarce, precluding its clinical application. In these sense, the use of new delivery systems that enhances EA bioavailability would improve the results already obtained. Also it remains to be determined if treatment with urolithins instead of EA would represent a better strategy in hepatic disease treatment.

传统药物或疗法极少影响慢性肝病的消退，这在许多情况下是由于持续的氧化应激所致。近年来，鞣花酸（EA）由于具有多种生物活性和多个分子靶点而受到关注。这是第一个侧重于肝保护方面的药理特性和由EA激活的分子机制的综述。EA具有抗氧化，抗肝毒性，抗脂肪性，抗胆汁生成，抗纤维化，抗肝癌和抗病毒特性，可改善肝脏的结构并抵抗毒性和病理性疾病。EA激活的分子机制包括清除自由基，调节I和II期酶，调节促炎性和纤维化细胞因子的合成，参与脂质合成和降解以及维持必需微量元素水平的生化途径的调控。EA还通过增加抗氧化反应，诱导细胞凋亡，下调参与细胞周期和血管生成的基因以及刺激细胞免疫反应来抑制肝星状细胞和肥大细胞的活化，转化细胞的增殖以及病毒复制。尽管EA作为一种创新的药理策略具有巨大的治疗潜力，但在患者中进行I和II期临床试验的数量仍然很少，这排除了其临床应用。从这些意义上讲，使用增强EA生物利用度的新递送系统将改善已经获得的结果。