Decursin is a phytochemical originally isolated from A. gigas with diverse biological activities.1,2,3,4,5 It reduces the growth of B16/F10 murine melanoma cells, but not NIH-3T3 fibroblasts, via induction of apoptosis and increased caspase-3 activity when used at concentrations ranging from 40 to 100 μM.1 In vivo, decursin (10 mg/kg, i.p.) reduces tumor growth in a B16/F10 mouse xenograft model. Decursin inhibits RANKL-induced osteoclast differentiation and decreases fusion and migrations of pre-osteoclasts in vitro and prevents LPS-induced bone erosion in mice.2 In a mouse model of seizures induced by kainic acid , decursin (20 mg/kg) increases latency to the first electroencephalographic (EEG) discharge and attenuates the intensity and reduces the frequency of seizure discharges in the parietal cortex.3 Decursin inhibits tube formation and expression of VEGF receptor 2 (VEGFR2) in human retinal microvascular endothelial cells (HRMECs) and human umbilical vein endothelial cells (HUVECs) in vitro and reduces retinal expression of VEGFR2 and neovascularization in rats with diabetes induced by streptozotocin .4 It also reduces hepatic collagen expression, serum levels of ALT, AST, and ALP, and production of reactive oxygen species (ROS) in a mouse model of CCL4-induced liver fibrosis.5
1.Kim, B.S., Seo, H., Kim, H.-J., et al.Decursin from Angelica gigas nakai inhibits B16F10 melanoma growth through induction of apoptosisJ. Med. Food.18(10)1121-1127(2015) 2.Kim, K.-J., Yeon, J.-T., Choi, S.-W., et al.Decursin inhibits osteoclastogenesis by downregulating NFATc1 and blocking fusion of pre-osteoclastsBone81208-216(2015) 3.Lee, J.-K., Jeong, J.W., Jang, T., et al.Decursin attenuates kainic acid-induced seizures in miceNeuroreport25(16)1243-1249(2014) 4.Yang, Y., Yang, K., Li, Y., et al.Decursin inhibited proliferation and angiogenesis of endothelial cells to suppress diabetic retinopathy via VEGFR2Mol. Cell. Endocrinol.378(1-2)46-52(2013) 5.Choi, Y.J., Kim, D.H., Kim, S.J., et al.Decursin attenuates hepatic fibrogenesis through interrupting TGF-beta-mediated NAD(P)H oxidase activation and Smad signaling in vivo and in vitroLife Sci.108(2)94-103(2014)