The anti-inflammatory effects of escin involve significant downregulation of expression of certain inflammatory genes, and upregulation of expression of granulocyte-macrophage colony-stimulating factor (GM-CSF), which also confers neuroprotection (1).
One of the mechanisms by which escin reduces chronic venous insufficiency is thought to be via inhibition of elastase and hyaluronidase, both involved in enzymatic proteoglycan degradation, which constitutes part of the capillary endothelium and is also the main component of the extravascular matrix (19).
The contraction of veins and arteries by horse chestnut is believed, partially, to be mediated through 5-HT(2A) receptors; horse chestnut also reduced platelet aggregation in vitro (20).
Beta-aescin and 5-fluorouracil were reported to inhibit human hepatocellular carcinoma SMMC-7721 cells, which may be due to the synergistic effects including cell-cycle arrest, induction of apoptosis, activation of caspases-3, 8 and 9, and down-regulation of Bcl-2 expression (17). In another study, escin was shown to potentiate the efficacy of gemcitabine, partially due to the inhibition of the nuclear transcription factor (NF-κB) activity and consequent inhibition of c-Myc, COX-2, Cyclin D1, Survivin, Bcl-2 and Bcl-xL, and the activation of caspase-3 (18).