Histological and Biochemical study of Nigella Sativa Seeds effects on Liver of male Albino Rats treated with Rifampicin

Abstract

Rifampicin (RF) considered a hepatotoxic drug. Is one of the first line successful drugs of management of tuberculosis. To reduce injury and protect liver from adverse effect of Rifampicin, this study was designed to investigate the activity of Nigella Sativa (NS) seeds powder aqueous suspension to hepato protection against Rifampicin.
For conducting this study,24 male albino rats were divided into four groups and all treated orally as follow; group І (control), received normal saline alone; group II, received RF (50mg/kg body weight/day); group III received NS it's called normal dose, (2g/kg body weight day); group IV RF (50mg/kg body weight) + NS (2g/kg body weight).Respectively for 28 days. Blood samples obtained for estimation of liver foundation parameters and enzymes such as serum alkaline phosphate (ALP), serum glutamic pyruvic transaminase (SGPT), serum glutamic Oxaloacetic transaminase (SGOT) and serum bilirubin. After rats were scarified, liver tissue sections were prepared for histopathological examination. The results parameters in treated rats in group II showed a significant (P<0.05) increase, while group IV showed a significant (P<0.05) decrease in biochemical parameters of liver. Liver histopathological examination of animal group treated with RF showed focal necrotic area in the hepatocyte and neutrophils and mononuclear cells aggregation in thickening wall of congested blood vessels with large granulomatous lesion in liver Parenchyma.
The Histological examination of pre-treatment animal group of NS (2g/kg body weight) showed near normal liver architecture with moderate aggregation of mononuclear cell around blood vessels and moderate proliferation of kupffer cells.
Pre-treatment of NS produced significant hepatoprotection by decreasing the levels of ALP, SGOT, SGPT and bilirubin. The result indicates clearly that NS possesses hepatoprotective and activity against RF induced hepato toxicity.