Research studies conducted in the laboratory have investigated the properties of silymarin or its isomer silybin using cell lines and animal models. Other substances in milk thistle have not been extensively studied.
Several research studies have investigated the effects of silymarin or silybin in a noncancer context. These studies have tested silymarin or silybin:
Caregivers usually define the onset of caregiving as the time of the patient's first cancer diagnosis; ideally, interventions for the caregiver should begin then. However, no validated model exists that can be applied to understanding the family caregiver experience, and few settings perform routine caregiver assessment-making the job of oncology practitioners more difficult, as they have no suitable framework for guiding their care decisions.
Generally speaking, interventions for the caregiver...
In stimulating detoxification pathways (enzyme concentrations and activity).
For antioxidant properties.
Silymarin or silybin has also been investigated in cancer models. The effects of silymarin and/or silybin have been investigated in prostate (DU 145, LNCaP, PC-3),[1,2,3,4,5,6]breast (MDA-MB 468, MCF-7),[7,8,9]hepatic (HepG2),[10,11] epidermoid (A431),colon (Caco-2),ovarian (OVCA 433, A2780),histiocytic lymphoma (U-937), and leukemia (HL-60) [15,16]cells. In animal tumor models, tongue cancer, skin cancer,[18,19,20,21,22,23]bladder cancer, and adenocarcinoma of the colon [25,26] and small intestine have been investigated. These studies have tested the ability of silymarin or silibinin to:
Mitigate the toxicity associated with chemotherapy agents.
Enhance the efficacy of chemotherapy agents.
Inhibit the growth of cancer cell lines and inhibit tumor initiation or tumor promotion.
Although many of these studies have produced encouraging results, none of the findings have been replicated in human clinical trials.
Laboratory data suggest that silymarin and silybin protect the liver from damage induced by toxic chemicals. Animal studies have found that liver cells treated with silybin and then exposed to toxins do not incur cell damage or death at the same rate as liver cells that are not treated with silybin. This finding suggests that silybin can prevent toxins from entering the cell or effectively exports toxins out of the cell before damage ensues.[11,27,28,29,30,31] Alternatively, this may be related to the effect of silymarin on detoxification systems. In vitro data have shown silybin to stimulate and/or inhibit phase I detoxification pathways in silybin-treated human liver cells. However, this effect was found to be dose-dependent, and these levels are not physiologically attainable with the current manufacturer dose recommendations.[32,33]
Silymarin has been shown to stimulate phase II detoxification pathways in mice. Administration of silymarin (100 or 200 mg/kg body weight/day) to SENCAR mice for 3 days significantly increased glutathione S-transferase activity in the liver (P < .01-.001), lung (P < .05-.01), stomach (P < .05), small bowel (P < .01), and skin (P < .01). This effect appeared to be dose-dependent. Administration of silymarin to rats challenged with a toxin (50 mg/kg body weight) resulted in higher levels of glutathione in liver cells, decreased levels of oxidative stress (measured by malondialdehyde concentrations), and less elevated liver function tests (measured by levels of aspartate aminotransferase [AST] and alanine aminotransferase [ALT]). Silymarin and silybin have also been found to accelerate cell regeneration in the liver through stimulation of precursors to DNA synthesis and enhancement of production of the cellular enzymes required for synthesis of DNA.[35,36,37,38,39,40] Laboratory studies have also shown silymarin and silybin to be potent antioxidants.[28,29,41,42,43,44,45,46,47,48] Silymarin has been shown to mitigate oxidative stress in cells treated with pro-oxidant compounds.