Siliver

Silymarin hepatoprotective effects are accomplished both directly and indirectly. The primary actions are as follows:
Sliliver – Hepatocellular Protection
Silymarin, and more specifically silibinin, directly aids hepatocytes by binding to the outside of the cells and blocking the binding of potential hepatocellular toxins. This was first noted in experimental studies investigating toxins from Amanita phalloides (death cap mushroom). Ingesting this mushroom causes swift and severe damage to hepatocytes. Silymarin blocks the receptor sites by which the mushroom toxins enter the cells. In addition, toxins that have already penetrated hepatocytes are neutralized by silibinin. In animal studies, silymarin given within 10 minutes after Amanita toxin ingestion completely counteracted the toxic effects, and if given within 24 hours of toxin ingestion silymarin prevented death and greatly reduced liver damage. Similar hepatoprotective effects have been shown in invitro and animal studies against ethanol and acetaminophen.
Siliver – Antioxidant Activity
Silymarin acts as a free radical scavenger and has been noted to increase production of glutathione in hepatocytes. Silymarin has been shown in one animal study to raise intracellular glutathione level by as much as 50 percent. Silymarin also increases the activity of superoxide dismutase in erythrocytes.
Siliver- Regenerative Properties
Silymarin stimulates the regenerative ability of the liver to form new hepatocytes by stimulating the activity of DNA-dependent RNA-polymerase I. This results in an increase in rRNA synthesis and increased protein synthesis. In vitro studies suggest this action extends only to normal hepatocytes and not cancerous cells.
Siliver -Antifibrotic Activity
The ability of silymarin to block fibrosis in the liver was first shown in a study with rats
subjected to complete bile duct occlusion.This action was later demonstrated in an open label, uncontrolled study of 998 patients with liver disease due to a variety of factors, including alcohol abuse, chronic active hepatitis B or C, drugs, and chemical exposure. Use of 140 mg of silymarin (equivalent to approximately 60 mg of silibinin) three times daily for three months led to a significant reduction in amino terminal procollagen III peptide (PIIINP), a marker of fibrosis. In 19 percent of the patients, this measure had dropped to the normal range expected for a healthy person.