Randomized controlled trial of silymarin treatment in patients with cirrhosis of the liver

Ferenci, Péter; Dragosics, B; Dittrich, H.; Frank, Hugh A.; Benda, L; Lochs, Herbert; Meryn, Siegfried; Base, Wolfgang; Schneider, Barbara

doi:10.1016/0168-8278(89)90083-4

Cited by 442 publications

(245 citation statements)

References 13 publications

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“…was performed to determine the effect of silymarin in patients with cirrhosis (Ferenci et al, 1989). It was a randomized controlled study comprising 170 patients with cirrhosis.…”

Section: Liver Cirrhosismentioning

confidence: 99%

Milk thistle in liver diseases: past, present, future

Abenavoli

Capasso²,

Milić

et al. 2010

Phytotherapy Research

504

350

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Silybum marianum or milk thistle (MT) is the most well‐researched plant in the treatment of liver disease. The active complex of MT is a lipophilic extract from the seeds of the plant and is composed of three isomer flavonolignans (silybin, silydianin, and silychristin) collectively known as silymarin. Silybin is a component with the greatest degree of biological activity and makes up 50% to 70% of silymarin. Silymarin is found in the entire plant but it is concentrated in the fruit and seeds. Silymarin acts as an antioxidant by reducing free radical production and lipid peroxidation, has antifibrotic activity and may act as a toxin blockade agent by inhibiting binding of toxins to the hepatocyte cell membrane receptors. In animals, silymarin reduces liver injury caused by acetaminophen, carbon tetrachloride, radiation, iron overload, phenylhydrazine, alcohol, cold ischaemia and Amanita phalloides. Silymarin has been used to treat alcoholic liver disease, acute and chronic viral hepatitis and toxin‐induced liver diseases. Copyright © 2010 John Wiley & Sons, Ltd.

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“…was performed to determine the effect of silymarin in patients with cirrhosis (Ferenci et al, 1989). It was a randomized controlled study comprising 170 patients with cirrhosis.…”

Section: Liver Cirrhosismentioning

confidence: 99%

Milk thistle in liver diseases: past, present, future

Abenavoli

Capasso²,

Milić

et al. 2010

Phytotherapy Research

504

350

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“…1A) is isolated from the seeds of Silybum marianum, a tall herb with prickly leaves and a milky sap. It has been clinically used as an antihepatotoxic agent for many liver diseases (7,8). Recent reports have shown that silibinin also has therapeutic aspects to reduce biliary cholesterol levels, intervene in hormone refractory human prostate cancer, and decrease the nephritic effects of chemical injury (9).…”

Section: Introductionmentioning

confidence: 99%

Silibinin Protects Against Isoproterenol-Induced Rat Cardiac Myocyte Injury Through Mitochondrial Pathway After Up-regulation of SIRT1

Zhou

Li-jun

et al. 2006

J Pharmacol Sci

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Abstract. Terminally differentiated adult injured cardiac myocytes have been used for various animal models of heart failure. It has recently been shown that isoproterenol induces injury in rat neonatal cardiac myocytes via a β-adrenergic pathway, suggesting that it might be one of the factors involved in myocardial cell injury in heart failure in vivo. In the study, silibinin, a plant flavanoid from milk thistle was first evaluated for its protective effect against β-adrenergic agonist isoproterenol-induced injury in cultured rat neonatal cardiac myocytes. The viability, activation of lactate dehydrogenase (LDH), and content of maleic dialdehyde (MDA) were chosen for measuring the degree of cardiac myocytes injury. As a result, silibinin protected isoproterenol-treated rat cardiac myocytes from death and significantly decreased LDH release and MDA production. Silibinin increased superoxide dismutase activity, decreased [Ca 2+ ] i , and increased mitochondrial membrane potential (∆Ψ). Furthermore, the release of pro-apoptotic cytochrome c from mitochondria was reduced by silibinin. Silibinin increased the expression of anti-apoptotic Bcl-2 family protein Bcl-2, and up-regulation of SIRT1 inhibited the translocation of Bax from cytoplasm to mitochondria, which caused mitochondrial dysfunction and cell injury. These results demonstrate that silibinin protects against isoproterenol-induced cardiac myocytes injury through resuming mitochondrial function and regulating the expression of SIRT1 and Bcl-2 family members.

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“…Thus, the therapeutic activities of silibinin are based on a variety of potentially protective effects. The phenolic structure, for example, makes silibinin a radical scavenger, although it also has membrane-stabilising and regenerative properties (Faulstich et al, 1980;Ferenci et al, 1989;Sonnenbichler and Zetl, 1986). It is currently difficult to assess which of the properties of the flavonoid are responsible for the protection observed in this study.…”

Section: Discussionmentioning

confidence: 99%

Silibinin protects against cisplatin-induced nephrotoxicity without compromising cisplatin or ifosfamide anti-tumour activity

Bokemeyer

Fels²,

Dunn³

et al. 1996

Br J Cancer

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Summary Cisplatin is one of the most active cytotoxic agents in the treatment of testicular cancer, but its clinical use is associated with side-effects such as ototoxicity, neurotoxicity and nephrotoxicity. Long-term kidney damage from cisplatin particularly affects the proximal tubular apparatus and can be detected by increased urinary excretion of brush-border enzymes, such as L-alanine-aminopeptidase (AAP), and magnesium. In the current study, the flavonoid silibinin was used as a nephroprotectant for cisplatin-induced nephropathy in a rat animal model. Infusion of silibinin before cisplatin results in a significant decrease in glomerular (indicated by creatinine clearance and serum urea level) and tubular kidney toxicity (excretion of brush-border enzymes and magnesium). Silibinin given alone had no effect on renal function. In order to exclude an inhibition of the anti-tumour activity of cisplatin and 4-hydroperoxy-ifosfamide by coadministration of silibinin, in vitro studies were performed in three established human testicular cancer cell lines. Dose-response curves for cisplatin (3-30 000 nmol) combined with non-toxic silibinin doses (7.25 x 10-6 or 7.25 x 10-5 mol 1-1) did not deviate significantly from those of cisplatin alone as measured by relative cell survival during a 5 day assay using the sulphorhodamine-B staining technique. Also silibinin did not influence the cytotoxic activity of 4-hydroperoxy-ifosfamide (30-10 000 nmol) in vitro. In summary, these in vitro data rule out a significant inhibition of the anti-tumour activity of the major nephrotoxic components, cisplatin and 4-hydroperoxy-ifosfamide, by co-administration of silibinin in a human germ cell tumour cell line model. Together with these demonstrated cytoprotection effects in the rat animal model, these data form the basis for a randomised clinical trial of silibinin for the protection of cisplatin-associated nephrotoxicity in patients with testicular cancer.

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Randomized controlled trial of silymarin treatment in patients with cirrhosis of the liver

Cited by 442 publications

References 13 publications

Milk thistle in liver diseases: past, present, future

Milk thistle in liver diseases: past, present, future

Silibinin Protects Against Isoproterenol-Induced Rat Cardiac Myocyte Injury Through Mitochondrial Pathway After Up-regulation of SIRT1

Silibinin protects against cisplatin-induced nephrotoxicity without compromising cisplatin or ifosfamide anti-tumour activity

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