An updated review at molecular pharmacological level for the mechanism of anti-tumor, antioxidant and immunoregulatory action of silibinin.
- Author:
Hong-jun WANG
1
;
Yuan-yuan JIANG
;
Ping LU
;
Qiong WANG
;
Takashi IKEJIMA
Author Information
1. China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, Shenyang 110016, China.
- Publication Type:Journal Article
- MeSH:
Amyloid beta-Peptides;
metabolism;
Animals;
Anti-Inflammatory Agents;
pharmacology;
Antineoplastic Agents, Phytogenic;
pharmacology;
Antioxidants;
pharmacology;
Enzyme Activation;
Free Radical Scavengers;
pharmacology;
Humans;
Milk Thistle;
chemistry;
Molecular Structure;
NF-kappa B;
metabolism;
Protein-Tyrosine Kinases;
metabolism;
Reactive Oxygen Species;
metabolism;
Receptor Protein-Tyrosine Kinases;
metabolism;
Receptor, Epidermal Growth Factor;
metabolism;
Receptor, IGF Type 1;
metabolism;
Signal Transduction;
drug effects;
Silymarin;
chemistry;
isolation & purification;
pharmacology
- From:
Acta Pharmaceutica Sinica
2010;45(4):413-421
- CountryChina
- Language:Chinese
-
Abstract:
Silibinin, from milk thistle (Silybum marianum), is a flavonolignan with anti-oxidative and anti-inflammatory properties. It has been therapeutically used for the treatment of hepatic diseases in China, Germany and Japan. Recently, increasing evidences prove that silibinin is also a potent antitumor agent, and the major anti-tumor mechanism for silibinin is the prominent inhibition of the activities of receptor tyrosine kinases (RTKs) and their downstream signal molecules in a variety of tumor cell lines, such as epidermal growth factor receptor 1 (EGFR) and insulin-like growth factor 1 receptor (IGF-1R) signaling pathways. Meanwhile, the evidences that silibinin selectively scavenges hydroxyl free radical (*OH) and specifically inhibits the action of nuclear factor kappaB (NF-kappaB) provide more complicated explanations for its antioxidant and anti-inflammatory effects. Some new findings such as that silibinin attenuating the cognitive deficits induced by amyloid beta protein (Abeta) peptide through its antioxidative and anti-inflammatory properties is valuable to broad the medical prospect of silibinin. In this review, we discuss the molecular pharmacological mechanisms of silibinin, focusing on its inhibition of tyrosine kinases, actions of antioxidation, free radical scavenging, immunoregulation and anti-inflammation.
