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Most investigation has used standardised preparations of St Mary's thistle, the Silymarin constituent group or silybin. HEPATOPROTECTIVE EFFECT

Protection of liver cells has been demonstrated against the following substances in vitro or in vivo:

• carbon tetrachloride-induced liver cirrhosis (Chrungoo et al 1997, Mourelle et al 1989, Muriel & Mourelle 1990)

• paracetamol-induced liver peroxidation (Chrungoo et al 1997, Muriel et al 1992) St Mary's thistle 1039

• cyclosporin (von Schonfeld et al 1997)

• phenothiazine (Palasciano et al 1994)

• butyrophenone (Palasciano et al 1994)

• erythromycin (Davila etal 1989)

• amitriptyline and nortriptyline (Davila et al 1989)

• oestradiol (Morazzoni & Bombardelli 1995)

• amanita phalloides (Floersheim 1976, Vogel et al 1984)

• tacrine (Galisteo etal 2000)

• iron overload (Masini et al 2000, Pietrangelo et al 1995). The exact mechanism of action has not been fully elucidated; however, several observations have been made.

Toxin blockade Silymarin and silybin alter the structure of hepatocyte cell membranes by being incorporated into the hydrophobic-hydrophilic interface of the microsomal bilayer (Parasassi et al 1984). Additionally, inhibition of cyclic AMP-dependent phosphodiesterase by silybin has been shown in vitro, which results in increased cAMP and stabilisation of lysosomal membranes (Koch et al 1985). Both actions alter cell membrane function and may be important for protecting the cell from toxin-induced damage. Alternatively, components in St Mary's thistle may bind to the hepatocyte cell membrane receptor site and inhibit binding of toxins to these sites (Jacobs etal 2002).

Antioxidant activity Both a direct and an indirect free radical scavenging activity has been observed, with silymarin shown to increase the redox state and total glutathione content of the liver, intestine and stomach in vivo (Liu et al 2001, Gonzalez-Correa et al 2002, Hagymasi et al 2002, Valenzuela et al 1989). As such, enhanced antioxidant activity further adds to the herb's hepatoprotective effects, particularly when hepatic injury involves free radical molecules. Chelates iron Hepatic iron toxicity and fibrosis due to iron overload is mediated by lipid peroxidation of biological membranes and the associated organelles (Masini et al 2000). Both silymarin and silybin demonstrate protective effects against hepatic iron toxicity in vivo, primarily owing to antioxidant mechanisms. However, there is some evidence that iron chelation may also be involved (Borsari et al 2001, Masini et al 2000, Pietrangelo et al 1995, Psotova et al 2002).

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