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OBJECTIVE To present study was designed to investigate the hepatoprotective effect of epigallocatechin gallate(EGCG)in experimentally induced liver dysfunction in rats.METHODS Rats were administered paracetamol(3g·kg-1,po)on 3rd and 5th day to 7d of experiment to produce hepatotoxicity in Wistar rats.The atractyloside(MPTP opener)was administered at the dose(5mg·kg-1,po)for 7d.RESULTS Paracetamol caused increase in SGPT,SGOT,bilirubin,TBARS and decrease in SOD level in rats.However,pretreatment with EGCG(40mg·kg-1 po)in paracetamol group significantly reversed the effect of this hepatotoxicant and further resulted in decrease inflammatory cell infiltration,vacuolization and centrilobular necrosis as revealed by histological findings of rat liver in present study.Atractyloside(a selective MPTP opner)at the dose of 5mg·kg-1,po was given with EGCG for 7d in paracetamol treated rats.Treatment with EGCG and atractyloside significantly a bolished the hepatoprotective effect of EGCG in paracetamol treated rats when compared with EGCG pretreated paracetamol group.CONCLUSION The finding of present investigation may conclude that paracetamol causes severe liver damage which is characterized by increased oxidative stress and mitochondrial dysfunction due to opening of MPTP.This study demonstrates the heptoprotective potentiation of EGCG may be due to cellular protective mechanisms like preventing the opening of MPTP,anti-oxidative,anti-inflammatory,membrane stabilization effects in paracetamol induced hepatotoxicity in rats.
OBJECTIVE To present study was designed to investigate the hepatoprotective effect of epigallocatechin gallate (EGCG) in experimentally induced liver dysfunction in rats. METHODS Rats were administered paracetamol (3 g · kg -1, po) on 3rd and 5th day to 7d of experiment to produce hepatotoxicity in Wistar rats. atractyloside (MPTP opener) was administered at the dose (5 mg · kg -1, po) for 7d.RESULTS Paracetamol caused increase in SGPT, SGOT, bilirubin, TBARS and decrease in SOD level in rats. pretreatment with EGCG (40 mg · kg-1 po) in paracetamol group-bited reversed effect of this hepatotoxicant and further resulted in decreased inflammatory cell infiltration, vacuolization and centrilobular necrosis as revealed by histological findings of rat liver in present study. Atractyloside (a selective MPTP opner) at the dose of 5 mg · kg -1, po was given with EGCG for 7d in paracetamol treated rats. Treatment with EGCG and atractyloside significantly a bolished the hepatoprotective effect of EGCG in pa racetamol treated rats when compared with EGCG pretreated paracetamol group. CONCLUSION The finding of present investigation may conclude that paracetamol causes severe liver damage which is characterized by increased oxidative stress and mitochondrial dysfunction due to opening of MPTP. This study demonstrate the heptoprotective potentiation of EGCG may be due to cellular protective mechanisms like preventing the opening of MPTP, anti-oxidative, anti-inflammatory, membrane stabilization effects in paracetamol induced hepatotoxicity in rats.