protective effect of Nigella sativa oil against paracetamol induced hepatotoxicity in albino rats

ABSTRACT

The present work was performed to study the possible protective effect of Nigella sativa Oil [NSO] on hepatotoxicity induced by paracetamol, as a model of hepatotoxic agents. 50 adult male albino rats were used in this study, each rat weighing 120-150 grams. Animals were divided into 5 groups; 10 rats each group. Group [I] received saline intraperitoneal and served as control. Group [II] received paracetamol in a single dose 1 gm/kg intraperitoneally to each rats. Group [III] received Nigella sativa Oil [NSO] in a dose of 800 mg/kg orally daily for 4 weeks. Group [IV] rats of this group received Nigella sativa Oil orally once daily in a dose of 800 mg/kg for 4 weeks followed by a single dose of paracetamol i.p. [1 gm/kg]. Group [V] received a single dose of paracetamol [1 gm/kg] i.p followed by Nigella sativa Oil orally 800 mg/kg daily for 4 weeks. At the end of experiment all animals were sacrificed after an overnight fasting, and blood samples were collected for the biochemical ssessment of the standard liver function tests, serum transaminases [ALT, AST], alkaline phosphatase, total proteins and albumin. Malondialdehyde and glutathione were estimated in liver tissues in addition to histopathological examination of liver was performed in each group. The results of the present study showed that in group II there was a marked elevation of serum transaminases and decrease in total protein and albumin plus elevation of malondialdhyde and reduction of glutathione in liver tissues. Administration of NSO before or after paracetamol produced significant reduction in all parameters of liver function tests, also malondialdehyde in liver tissue decreased while glutathione showed a significant increase in liver tissues. Also there was an improvement in histopathological finding of the liver. The results of our study showed that Nigella sativa Oil can significantly protect and treat the liver against paracetamol-induced hepatotoxicity