Silibinin (Silybin), an effective anti-cancer and chemopreventive agent, has been shown to exert multiple effects on cancer cells, including inhibition of both cell proliferation and migration. In Vitro: Silibinin (Silybin) significantly induced the expression of the non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1) in both p53 wild-type and p53-null cancer cell lines^[1].
Silibinin (Silybin) induced cell death in human breast cancer cell lines MCF7 and MDA-MB-231^[2].
Silibinin (Silybin) treatment resulted in a dose- and time-dependent inhibition of HCC cell viability^[3].
Silibinin (Silybin) treatment decreased the expression of the Notch1 intracellular domain (NICD), RBP-Jκ, and Hes1 proteins, upregulated the apoptosis pathway-related protein Bax, and downregulated Bcl2, survivin, and cyclin D1^[3].
In Vivo: Topical application of silibinin at the dose of 9 mg/mouse effectively suppressed oxidative stress and deregulated activation of inflammatory mediators and tumorigenesis^[4].
The kidney cortex of vehicle-treated control OVE26 mice displayed greater Nox4 expression and twice as much superoxide production than cortex of silybin-treated mice. The glomeruli of control OVE26 mice displayed 35% podocyte drop out that was not present in the silybin-treated mice^[5].