Pathophysiology of cholesterol gallstone disease

The purpose of the present paper is to review the current knowledge about cholesterol gallstone disease. It is generally accepted that the formation of cholesterol gallstone requires three major pathogenic defect, namely, supersaturation, nucleation and crystal growth as well as disorder of gallbladder motility. The supersaturation is necessary but not sufficient to explain stone formation. It has been suggested that nucleation is the key factor for gallstone formation. However, those three factors are necessary for the formation of cholesterol gallstones, and the presence of just one or two factor does not lead to stones. We also touch briefly on the results form studies performed in Mexico in this area

Anticholestatic effect of picroliv, active hepatoprotective principle of Picrorhiza kurrooa, against carbon tetrachloride induced cholestasis.

Picroliv showed a dose (3-12 mg/kg, po for 7 days) dependent choleretic activity as evidenced by increase in bile flow and its contents (bile salts and bile acids). Significant anticholestatic activity was also observed against carbon tetrachloride induced cholestasis in conscious rat, anaesthetized guinea pig and cat. Picroliv was more active than the known hepatoprotective drug silymarin.