Quercetin is a flavonoid present in Artemisia scopunu (AS) and some other plants [l]. It possesses anti-inflammatory [2] antioxidant and free radical scavenging [3], anti-tumor [4] and calcium antagonist [5] activities. AS has been used traditionally to correct liver damage. In our previous studies, we demonstrated that this folkmedical use had scientifically justified basis as the crude extract of this plant showed hepatoprotective activity in an animal model of hepatotoxicity [6]. The aim of this investigation was to see whether quercetin exhibits hepatoprotective activity, which may explain the folkloric use of this plant in hepatitis.

Swiss male mice (20-25 g) and male albino Wistar rats (200-250 g) housed at the Animal House of The Aga Khan University, maintained at 23-25 C were used for this study. Preliminary experiments were performed on mice to estimate the protective effect of quercetin against lethal dose of paracetamol (1 glkg). Animals were divided into 2 groups of 10 animals each. One group was treated orally with quercetin (10 mg/kg) followed after one hour by oral administration of paracetamol (1 g/kg). The second group served as a control and received same treatment except that normal saline (0.9% NaCI) was administered instead of test drug. The mortality was observed for 24 hrs post-administration of paracetamol. Hepatic injury was produced by oral administration of paracetamol (640 mg/Kg) suspended in 1% methylcellulose. Rats were divided into 3 groups each containing 10 animals. Group 1 served as vehicle control and received normal saline and vehicle orally. Group 2 received 4 doses of normal saline (10 ml/kg) at 12 hrs interval and paracetamol was administered orally one hr post-treatment of the last dose. Group 3 was treated similar to the group 2 except that quercetin (10 mg/kg) was administered instead of saline. Animals were anaesthetized with ketamine (100 mg/Kg, im) 24 hrs after the last treatment and blood (3 mL) was collected by cardiac puncture using sterile disposable syringes. Serum was separated by centrifugation (3000 rpm, for 15 min) and serum aminotransaminases (GOT and GPT) were estimated on the same day spectrophotometrically using Merck diagnostic kits. Oral administartion of paracetamol produced 100% mortality at the dose of 1 g/kg in mice while pretreatment of animals with quercetin (10 mg/kg) reduced the death rate to 30%. Figure 1 shows the effect of quercetin on paracetamolinduced hepatotoxicity. Paracetamol (640 mg/Kg; orally) produced liver damage in rats as manifested by significant rise (P< 0.05) in serum GOT and GPT to 813 f 158, 475 f 124 IU/L (mean f SEM; n= 10) respectively compared to respective control values of 89 f 13 and 41 f 10. Pretreatment of rats with quercetin (10 mg/kg; orally) lowered significantly (P< 0.05) the respective serum GOT and GPT levels to 105 f 11 and 46 f 09. Liver injury induced by paracetamol is commonly used models for theweening of hepatoprotective drugs [7l. The rise in serum levels of transaminases has been attributed to the damaged structural integrity of the liver because these are cytoplasmic in location and are released into circulation after cellular damage [8]. Quercetin seems to preserve the structural integrity of the hepato-cellular membrane. This was evident from the protection provided to mice against lethal dose of