COMPARATIVE STUDIES ON THE EFFECT OF TURMERIC AND GINGER AGAINST PARACETAMOL INDUCED LIVER DAMAGE IN FEMALE ALBINO RATS
Olushola Ladeji, Sangodele J. O, Chinenye Egwuonwu, Ijeoma B. Eluwa
ABSTRACT
The present study was conducted to evaluate and compare the effect of the ethanol extract of Curcuma longa and Zingiber officinale against paracetamol induced liver damage in female albino rats. 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Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally ( 1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally ( 1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally ( 1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally ( 1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally ( 1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally ( 1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control given normal saline orally (1ml/kg). Group B served as the positive control paracetamol treated group) in which the rats were treated orally with paracetamol at dose of 400mg/kg body weight for 7 days. Group C was pretreated with a standard drug, silymarin -200mg/kg plus paracetamol for 7 days. Group D and E were pretreated with turmeric extract (200mg/kg and 400mg/kg respectively) prior to paracetamol treatment. Group F and G were pretreated with ginger extract (200mg/kg and 400mg/kg respectively) prior to the administration of paracetamol simultaneously for 7 days. Paracetamol, normal saline and the extracts were administered orally, once daily. Paracetamol at 400mg/kg induced liver damage in rats, manifested by statistically increased serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin and thiobarbutiric acid reactive substances, also reduced total serum protein. Pre-treatment of rats with ethanolic extracts of Curcuma longa and Zingiber officinale prior to paracetamol dosing lowered serum liver enzyme activities, bilirubin, thiobarbituric acid reactive substances and increased total serum protein. It was concluded from the result that the ethanolic extracts of Curcuma longa and Zingiber officinale posses hepatoprotective activity against paracetamol induced liver damage, with Curcuma longa (turmeric) having a higher potential when compared with Zingiber officinale (ginger).
Keywords: paracetamol, Zingiber officinale, thiobarbutiric, hepatoprotective.
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