Silibinin health benefit
March 4 2016 by
Ray Sahelian, M.D.


Silibinin is a flavonolignan found in certain herbs, particularly milk thistle. Silibinin is a strong antioxidant and modulates the insulin-like growth factor (IGF) system by increasing circulating levels of IGF-binding protein 3 (IGFBP-3) and decreasing levels of IGF-I. In preliminary studies, silibinin has been tested in various cancers including lung, colon, oral, and prostate.


Breast cancer
Int J Pharm. 2013 . Synergistic Inhibition of Breast Cancer Metastasis by Silibinin Loaded Lipid Nanoparticles Containing TPGS.


Colon Cancer
Pilot study of oral silibinin, a putative chemopreventive agent, in colorectal cancer patients: silibinin levels in plasma, colorectum, and liver and their pharmacodynamic consequences.
Clin Cancer Res. 2006. Cancer Biomarkers and Prevention Group, Department of Cancer Studies, University of Leicester, United Kingdom.
Patients with confirmed colorectal adenocarcinoma received silibinin formulated with phosphatidylcholine (silipide) at dosages of 360, 720, or 1,440 mg silibinin daily for 7 days. Blood and biopsy samples of normal and malignant colorectum or liver were obtained before dosing, and blood and colorectal or hepatic tissues were collected at resection surgery after the final silipide dose. Levels of silibinin were quantified by high-pressure liquid chromatography-UV, and plasma metabolites were identified by liquid chromatography-mass spectrometry. Silibinin monoglucuronide, silibinin diglucuronide, silibinin monosulfate, and silibinin glucuronide sulfate were identified in the plasma. Intervention with silipide did not affect circulating levels of IGFBP-3, IGF-I, or M1dG. The high silibinin levels achieved in the human colorectal mucosa after consumption of safe silibinin doses support its further exploration as a potential human colorectal cancer chemopreventive agent.


Nutr Hosp. 2014. Anti-proliferative action of silibinin on human colon adenomatous cancer HT-29 cells.


Silibinin and Lung Cancer
Silibinin, a substance derived from milk thistle, destroys lung cancer in mice. Milk thistle components, silymarin and silibinin, have been examined against different cancers for over a decade.In a study reported in the Journal of the National Cancer Institute, June 21, 2006, researchers injected mice with a chemical called urethane to induce lung cancer. The animals then received diets containing different doses of silibinin. Mice fed silibinin had fewer large lung tumors than untreated mice. Further analysis showed that silibinin seemed to reduce the number of blood vessels that provide nutrients to the tumors, allowing them to grow. Human trials of silibinin are already underway for the treatment of prostate cancer.


Carcinogenesis. 2015. Combinations of indole-3-carbinol and silibinin suppress inflammation-driven mouse lung tumorigenesis by modulating critical cell cycle regulators. The combination may be of benefit in lung cancer.


Nutr Cancer. 2013. Chemopreventive and anti-cancer efficacy of silibinin against growth and progression of lung cancer. The use of systemic chemotherapeutic drugs and molecular-targeted therapies in the treatment of patients with locally advanced or metastatic lung cancer has its limitations due to the associated acute and cumulative dose limiting toxicities and acquisition of drug resistance. Prevention and therapeutic intervention by dietary agents including nutraceuticals which are non-toxic, cost-effective, and physiologically bioavailable, are emerging approaches in lung cancer management. In this regard, silibinin, a natural flavonolignan, has been rigorously evaluated for the prevention and growth control of lung cancer through extensive in vitro and in vivo studies. Successful studies conducted so far, have established that silibinin is effective both alone and in combination with other agents (e.g., chemotherapeutic and epigenetic agents) in significantly inhibiting the growth of lung cancer cells. In vivo, its effects have been shown to be mediated through inhibition of proliferation, angiogenesis and epigenetic-related events. Therefore, the present review focuses on encompassing the efficacy and mechanisms of silibinin against lung cancer.


Prostate cancer prevention
Prostate cancer chemoprevention by silibinin: bench to bedside.
Mol Carcinog. 2006. Singh RP, Agarwal R. Department of Pharmaceutical Sciences, School of Pharmacy, University of Colorado at Denver and Health Sciences Center, Denver, Colorado
One approach to reduce PCA incidence, growth and metastasis is prevention and intervention targeted towards mitogenic and survival signaling and cell-cycle regulation. This approach is based on the rationale that overexpression of receptor tyrosine kinases (RTKs) and/or non-receptor tyrosine kinases leads to persistent autocrine stimulation of malignant cells for deregulated cell-cycle progression and uncontrolled growth. Silibinin inhibits growth of PCA cells from human, mouse, and rat origins, and also suppresses human prostate tumor xenograft growth in nude mice. Silibinin also inhibits PCA growth in the transgenic adenocarcinoma of mouse prostate (TRAMP) mouse model. Now, silibinin has been entered into phase I/II clinical trials in human PCA patients where preliminary observations were suggestive of its further study in a larger base of the patient population.


Silibinin inhibits invasion of oral cancer cells by suppressing the MAPK pathway.
J Dent Res. 2006.
Oral squamous cell carcinoma (OSCC) is the most common malignancy of the oral cavity. Here, we provide molecular evidence associated with the anti-metastatic effect of silibinin by showing a marked inhibition of the invasion and motility of SCC-4 tongue cancer cells by 100 muM of silibinin. These results suggested that silibinin can reduce the invasion and metastasis of tumor cells, and such a characteristic may be of great value in the development of a potential cancer therapy.


Parkinson's disease
Brain Res. 2015. Silibinin suppresses astroglial activation in a mouse model of acute Parkinson׳s disease by modulating the ERK and JNK signaling pathways.