Phenidone, a dual inhibitor of cyclooxygenase and lipoxygenase, inhibits carbon tetrachloride-induced acute liver injury in rats

  • Choi, Hyuop (College of Veterinary Medicine and Institute of Veterinary Science, Kangwon National University) ;
  • Joeng, Donghwan (College of Veterinary Medicine and Institute of Veterinary Science, Kangwon National University) ;
  • Jung, Bae-Dong (College of Veterinary Medicine and Institute of Veterinary Science, Kangwon National University) ;
  • Shin, Taekyun (College of Veterinary Medicine, Jeju National University) ;
  • Wie, Myung-Bok (College of Veterinary Medicine and Institute of Veterinary Science, Kangwon National University)
  • Accepted : 2010.06.05
  • Published : 2010.06.30

Abstract

This study was carried out to find whether phenidone (1-phenyl-3-pyrazolidinone), a cyclooxygenase as well as a lipoxygenase inhibitor, exhibits the preventive effect on carbon tetrachloride $(CCl_{4})-induced$ acute liver injury in rats. Rats were pretreated with phenidone at a dose of 50 or 200 mg/kg (p.o.) once daily for 3 consecutive days before $CCl_{4}$ administration. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Malondialdehyde (MDA) production was determined as an index of lipid peroxidation in the liver and serum. The histopathological changes in the liver were also examined in each group. The reduction in body weights was significantly inhibited in the phenidone-treated group than in the $CCl_{4}$ control group. Significant increase in the relative liver weights of the phenidone-treated groups was observed compared with either the vehicle or $CCl_{4}$ groups. Elevation of serum AST and ALT activities occurred after $CCl_{4}$ treatment was significantly attenuated by the pretreatment with phenidone. The elevation of MDA levels in liver and serum were completely inhibited in phenidone-treated groups. The protective effects on phenidone-treated groups were confirmed histopathologically. These results suggest that phenidone may be a useful protector through modulation of hepatic inflammation in $(CCl_{4})-induced$ acute liver injury.

Keywords

References

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