Milk thistle (silymarin) is a very cheap glutathione booster:
Inhibition of cyclooxygenase-2 and inducible nitric oxide synthase by silymarin in proliferating mesenchymal stem cells: comparison with glutathione modifiers.
Ahmadi-Ashtiani H, Allameh A, Rastegar H, Soleimani M, Barkhordari E.
Source
Department of Biochemistry, Faculty of Medical Sciences, Tarbiat Modares University, POB 14115-111, Tehran, Islamic Republic of Iran.
Abstract
Silymarin, a mixture of flavonolignans, is extracted from milk thistle (Silybum marianum) and has a strong antioxidant activity and exhibits anticarcinogenic, anti-inflammatory, and cytoprotective effects. In this study we attempted to determine whether silymarin and the glutathione modifiers, buthionine sulfoxamine (BSO) and N-acetylcysteine (NAC), are involved in regulation of cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) in proliferating mesenchymal stem cells (MSCs). Cellular glutathione was manipulated during a 14-day culture using BSO, NAC and silymarin. At intervals of 2, 7 and 14 days, cells were collected and COX-2 and iNOS levels were measured. In parallel, generation of cellular H(2)O(2) and glutathione were measured. Supplementation of the culture media with BSO caused a dose-dependent decrease in MSC proliferation, whereas NAC or silymarin elevated the proliferation (p < 0.05). Treatment of MSC with NAC or silymarin caused a significant decrease in COX-2 levels. However, COX-2 levels in cells treated with high levels of NAC (1.0 mM) were significantly lower than those in MSCs treated with high levels of silymarin (100 μM). BSO (1.0 and 5.0 μM) caused a significant increase in COX-2 on days 2, 7 and 14. BSO caused a significant increase in iNOS, whereas NAC or silymarin decreased cellular iNOS.
Overall result show that glutathione, iNOS and COX-2 in proliferating MSCs are affected by silymarin treatment. It appears that glutathione is the main target of silymarin, and in consequence iNOS and COX-2 are affected in response to silymarin treatment.
http://www.ncbi.nlm.nih.gov/pubmed/21710354
Indian J Med Res. 2006 Nov;124(5):491-504.
Hepatoprotective herbal drug, silymarin from experimental pharmacology to clinical medicine.
Pradhan SC, Girish C.
Source
Department of Pharmacology, Jawaharlal Institute of Postgraduate Medical Education & Research, Pondicherry, India.
scpradhan@jipmer.edu
Abstract
Silymarin, a flavonolignan from 'milk thistle' (Silybum marianum) plant is used almost exclusively for hepatoprotection and amounts to 180 million US dollars business in Germany alone. In this review we discuss about its safety, efficacy and future uses in liver diseases. The use of silymarin may replace the polyherbal formulations and will avoid the major problems of standardization, quality control and contamination with heavy metals or bacterial toxins. Silymarin consists of four flavonolignan isomers namely--silybin, isosilybin, silydianin and silychristin. Among them, silybin being the most active and commonly used. Silymarin is orally absorbed and is excreted mainly through bile as sulphates and conjugates. Silymarin offers good protection in various toxic models of experimental liver diseases in laboratory animals. It acts by antioxidative, anti-lipid peroxidative, antifibrotic, anti-inflammatory, membrane stabilizing, immunomodulatory and liver regenerating mechanisms. Silymarin has clinical applications in alcoholic liver diseases, liver cirrhosis, Amanita mushroom poisoning, viral hepatitis, toxic and drug induced liver diseases and in diabetic patients.
Though silymarin does not have antiviral properties against hepatitis virus, it promotes protein synthesis, helps in regenerating liver tissue, controls inflammation, enhances glucuronidation and protects against glutathione depletion. Silymarin may prove to be a useful drug for hepatoprotection in hepatobiliary diseases and in hepatotoxicity due to drugs. The non traditional use of silymarin may make a breakthrough as a new approach to protect other organs in addition to liver. As it is having a good safety profile, better patient tolerability and an effective drug at an affordable price, in near future new derivatives or new combinations of this drug may prove to be useful.
http://www.ncbi.nlm.nih.gov/pubmed/17213517
Comparative effects of silymarin and vitamin E supplementation on oxidative stress markers, and hemoglobin levels among patients on hemodialysis.
Roozbeh J, Shahriyari B, Akmali M, Vessal G, Pakfetrat M, Raees Jalali GA, Afshariani R, Hasheminasab M, Ghahramani N.
Source
Division of Nephrology, Department of Medicine, Nephro-Urology Research Center, Shiraz University of Medical Sciences, Shiraz, Islamic Republic of Iran.
Abstract
BACKGROUND:
The incidence of accelerated atherosclerosis among patients on hemodialysis is very high and oxidative stress (OS) is a potentially major contributor to their morbidity and mortality.
OBJECTIVE:
To evaluate the effects of Silymarin and/or vitamin E on OS markers and hemoglobin levels in patients on hemodialysis.
METHODS:
Eighty patients on hemodialysis were randomized into four groups: Group 1 received silymarin 140 mg 3 times daily; Group 2 received vitamin E 400 IU/day; Group 3 received silymarin 140 mg 3 times daily and vitamin E 400 IU/day; and Group 4 was the control. Samples were obtained at baseline and on
day 21 for measurement of malondialdehyde (MDA), red blood cell (RBC) glutathione peroxidase (GPX), and hemoglobin.
RESULTS:
Combination of silymarin and vitamin E led to a reduction in the MDA levels (7.84 ± 1.84 vs. 9.20 ± 2.74 nmol/mL; p = 0.008). There was a significant increase in RBC GPX levels in all treatment groups compared with controls after 3 weeks. This was more pronounced in the group receiving combination compared with the group receiving vitamin E or the control group (5.78 ± 3.51, 4.22 ± 1.63, and 3.16 ± 1.89 IU/grHb, respectively; p < 0.001). There was also a significant increase in mean hemoglobin of all treatment groups compared with the control.
CONCLUSIONS:
Oral supplementation with silymarin and vitamin E leads to reduction in MDA, increase in RBC GPX, and increase in hemoglobin levels in patients with end-stage renal disease. Studies with larger sample sizes and longer follow-up are required to investigate the effect of silymarin on cardiovascular outcomes and erythropoietin requirement.
http://www.ncbi.nlm.nih.gov/pubmed/21332331
Effects of silymarin on the proliferation and glutathione levels of peripheral blood mononuclear cells from beta-thalassemia major patients.
Alidoost F, Gharagozloo M, Bagherpour B, Jafarian A, Sajjadi SE, Hourfar H, Moayedi B.
Source
Department of Immunology, School of Medicine, Hezar Jerib Avenue, Isfahan University of Medical Sciences, Isfahan, Iran.
Abstract
Iron toxicity in beta-thalassemia major is the main cause of oxidative stress and cell mediated immune deficiencies. Despite indicative signs of severe oxidative deficiencies associated with beta-thalassemia major, such as decreased level of plasma antioxidants and depletion of erythrocyte glutathione, little is known about intracellular redox status of immune cells. Since glutathione is a primary intracellular antioxidant and plays an essential role in several functions in T cells, in this study intracellular glutathione (GSH) levels as well as proliferation of PHA-activated peripheral blood mononuclear cells (PBMC) were investigated in 28 beta-thalassemia major patients and 28 healthy age-matched individuals. Considering the potential benefits of flavonoids in the therapy of oxidative stress, the effects of silymarin on the GSH levels and proliferation of PBMC from normal and thalassemia individuals were further examined. Quantitative determination of intracellular GSH and proliferative response of PBMC to PHA were performed before and after 72 h incubation of PBMC with various concentrations of silymarin (0, 5, 10, or 20 mug/ml). Results demonstrated a significant reduction of GSH and proliferation in beta-thalassemia major cells; however treatment with silymarin led to restoration of both GSH levels and PBMC proliferation in thalassemia patients. Considerably low levels of GSH and depressed proliferative response of PBMC in beta-thalassemia major may be responsible for the cell mediated immune abnormalities in iron overload conditions
. Moreover, the GSH restoration and improvement of PBMC growth by silymarin is a possible explanation for its recently reported antioxidant and immunostimulatory activities. These data suggest the benefit of using flavonoids to normalize immune dysfunction in beta-thalassemia major. The immunomodulatory effects of silymarin in beta-thalassemia major are currently under further investigation in a double blind clinical trial.
http://www.ncbi.nlm.nih.gov/pubmed/16782543
There was also a study which showed that a topical formula of MSM and milk thistle were an effective treatment for rosacea (an inflammatory condition):
http://www.ncbi.nlm.nih.gov/pubmed/18254805
I subscribe and save to dis one:
http://www.amazon.com/gp/product/B0013OULVA/ref=ox_sc_sfl_title_9?ie=UTF8&smid=ATVPDKIKX0DER and take 2 or 3 a day.