engleski

Protection of acetaminophen-induced hepatotoxicity in mice by PGE2

Acetaminophen (AAP) administered to mice via gastric tube in a dose of 300-350 mg/kg induced heavy liver injury and killed 55% - 80% mice within 48 hours. Dimethyl-16-16 prostaglandin E2 (PGE2), given intraperitoneally (0.025-0.2 mg/kg) 15 to 30 minutes before AAP, ameliorated the liver injury and reduced the mortality in mice to 20%-30%. PGE2 also significantly reduced the increase in plasma transaminase (ALT, AST) levels induced by AAP. In the same doses, PGE1 had a slight but not significantly protective effect. When given 2 hours after AAP administration, PGE2 delayed the death of mice but had no significant effect on total mortality. Pretreatment of mice with indomethacin (4 mg/kg i.p.) had no effect on AAP toxicity, while pretreatment of mice with specific anti-PGE2 antibodies increased this toxicity. Thus, PGE2 was concluded to have a protective role in AAP-induced hepatotoxicity.

Prostaglandins E; Acetaminophen; Hepatitis; Toxic

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