"目录号: HY-13748
Silibinin为抗癌和化疗预防化合物，能抑制细胞增殖和迁移。
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Description
Silibinin, 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.IC50 value:Target: anticancerin vitro: silibinin 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, suggesting that silibinin-induced NAG-1 up-regulation is p53-independent manner.Silibinin up-regulates early growth response-1 (EGR-1) expression [1]. silibinin induced cell death in human breast cancer cell lines MCF7 and MDA-MB-231. Silibinininduced cell death was attenuated by antioxidants, N-acetylcysteine (NAC) and Trolox, suggesting that the effect of silibinin was dependent on generation of reactive oxygen species (ROS) [2]. SIL treatment resulted in a dose- and time-dependent inhibition of HCC cell viability, SIL exhibited strong antitumor activity, as evidenced not only by reductions in tumor cell adhesion, migration, intracellular glutathione (GSH) levels and total antioxidant capability (T-AOC) but also by increases in the apoptotic index, caspase3 activity, and reactive oxygen species (ROS). SIL 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. Notch1 siRNA (in vitro) or DAPT (a known Notch1 inhibitor, in vivo) further enhanced the antitumor activity of SIL, and recombinant Jagged1 protein (a known Notch ligand in vitro) attenuated the antitumor activity of SIL [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].
Clinical Trial
Medical University of Vienna
Hepatitis C
October 2007
Phase 2
Madaus Inc-Mylan Inc.
Amatoxin Poisoning-Amanita Poisoning-Mushroom Poisoning-Liver Failure
February 2010
Phase 2-Phase 3
University of Zurich
HIV-Hepatitis C
April 2013
Phase 2
Rottapharm
Hepatitis C, Chronic
August 2013
Phase 2-Phase 3
Rottapharm
HCV Recurrence After Liver Transplantation
September 2010
Phase 2
Rottapharm-Azienda Ospedaliera Universitaria Policlinico
Hepatitis C Virus Recurrence
August 2011
Phase 2
MedicalLogic-Kosin University Gospel Hospital
Carcinoma, Non-Small-Cell Lung
April 2014
Phase 2
University of Catania
Work Ability-Depression
February 2010
Phase 3
University of Catania
Liver Fibrosis
June 2010
Phase 3
Fundacion para la Investigacion Biomedica del Hospital Universitario Ramon y Cajal-Fundación Mutua Madrileña
Healthy Volunteers
October 2013
Phase 1
Abby Siegel-Lotte & John Hecht Memorial Foundation-Columbia University
Advanced Hepatocellular Carcinoma
February 2010
Phase 1
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