The protective effect of Nigella Sativa oil on Penconazole induced -renal toxicity in adult albino rats: Histological, Immunohistochemical and Biochemical study

Abstract

High doses of penconazole causing nephrotoxicity and renal damage. Nigella sativa (black seed) is one of the native plants. It has anti-inflammatory, antidiabetic and anti-cancerous properties.Aim: This work aimed to evaluate the effect of Nigella sativa oil on Penconazole induced renal toxicity in a rat model.Material and Methods: Sixty male adult albino rats were used . They were divided into equal four groups. Group I (control): rats were received distilled water Group II (N. sativa): rats were given orally 0.2ml N. sativa oil /100 g b. wt. three days/week for four weeks.Group III(PEN –treated): the animals were received intraperitoneally 67 mg penconazole /kg b. wt. three days/week for four weeks. Group IV(PEN+ N.sativa): rats were given penconazole (67 mg/kg b.w) and N. sativa oil (0.2ml/100 g) simultaneously three days weekly for four weeks. At the end of the experiment, kidney tissues were prepared for biochemical, immunohistochemical, light and electron microscopic studies.Results: Histological examination of penconazole treated group revealed glomerular atrophy, widening of the subcapsular space and hypercellularity of the glomerular cells. Detachment of podocytes and disruption of their processes resulted in impairment of the blood renal barrier. Tubular degeneration and necrosis were confirmed by significant decrease in Bcl2 immune marker. An increase in activity of intercalated cells of cortical collecting tubules was an indication of metabolic acidosis. Renal fibrosis was confirmed by an significant increase in α SMA and collagen fibers. Biochemical study revealed an increase in MDA level, decrease in both superoxide dismutase (SOD) and catalase (CAT).These changes were reserved by concomitant administration of Nigella sativa oil.Conclusion: The antioxidant properties of Nigella sativa could be attributed in ameliorating penconazole-induced nephrotoxicity in rats.