Aescin, a natural mixture of triterpenoid saponins isolated from the seed of horse chestnut, has been identified as the active principle. Its anti-inflammatory effects involve downregulation of inflammatory gene expression and upregulation granulocyte-macrophage colony-stimulating factor production, which also confers neuroprotection ⁽¹⁾.

Aescin may reduce chronic venous insufficiency via inhibition of elastase and hyaluronidase, both involved in enzymatic proteoglycan degradation, which constitutes part of the capillary endothelium and is the main component of the extravascular matrix ⁽¹⁹⁾. Contraction of veins and arteries with horse chestnut may be partially mediated through 5-HT(2A) receptors ⁽²⁰⁾. It also reduced platelet aggregation in vitro ⁽²⁰⁾.

Beta-aescin and 5-fluorouracil inhibited human hepatocellular carcinoma cells, perhaps via synergistic effects including cell-cycle arrest, induction of apoptosis, caspase-3, -8 and -9 activation, and Bcl-2 downregulation ⁽¹⁷⁾. Escin potentiated gemcitabine efficacy in part through NF-κB inhibition and consequent inhibition of c-Myc, COX-2, cyclin D1, survivin, Bcl-2, and Bcl-xL, and caspase-3 activation ⁽¹⁸⁾.