Decursin, identified as (+)-Decursin, serves as a potent anti-tumor agent with additional cytotoxic properties and the ability to activate protein kinase C significantly. It triggers apoptosis and causes cell cycle arrest in the G1 phase while reducing the expression of CDK2, CDK4, CDK6, and cyclin D1 proteins over 48 hours. Beyond its anti-tumor capacity, Decursin also displays anti-inflammatory and analgesic effects, inhibiting cell proliferation and migration[1].[2].[3].[4].
体内研究
In in vivo models, Decursin demonstrates anti-tumor activity at a dosage of 4 mg/kg, administered subcutaneously daily for four weeks in mice[2].
Additionally, at a dosage of 50 mg/kg via intrathecal injection three times at two-day intervals over six days, it exhibits analgesic properties in a mouse model of paclitaxel-induced peripheral neuropathy[3].
体外研究
In DU145 cells, Decursin exhibits a dose- and time-dependent inhibition of cell growth when administered in concentrations of 0, 25, 50, and 100 μM over periods of 24, 48, 72, and 96 hours[1].
Decursin not only induces apoptosis and G1 phase cell cycle arrest in DU145 cells but also leads to G1, S, and G2-M phase arrests in PC-3 cells[1].
Additionally, at concentrations of 0, 25, 50, and 100 μM over 24 and 48 hours, Decursin significantly decreases the levels of CDK2, CDK4, CDK6, and cyclin D1 protein in DU145 cells[1].
Further studies reveal that Decursin, at concentrations of 0, 5, 20, and 100 μM over seven days, inhibits both the proliferation and differentiation abilities of AC133+ cells[2]. It also dose-dependently blocks SDF-1α-induced activation of Akt, ERK1/2, and eNOS[2].
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