Hepatoprotective Effect of Nicotinamide Versus Lead-Motivated Hepatotoxicity in Rats via Correcting Effect on Nuclear Factor-kβ Pathway and Glutathione Metabolism

Abstract

Many years ago, until now, lead (Pb) poisoning is one of the pivotal environmental issues. Pb prompts liver dysfunction by elevating in ammation following oxidative stress. Consequently, we for the rst time investigated the effect of nicotinamide (B3) on the rat's liver histopathological and biochemical pro les in a rat model of Pb toxicity. Materials and MethodsThirty-six rats were shared into four groups (nine rats in each): untreated normal (N), B3 treated normal (N-B3), lead toxicity (Pbt), and B3 lead toxicity (Pbt-B3). Treated groups took B3 (180 mg/L in drinking water for one month). Pb intoxication was motivated in rats by acquiring 50 mg/l lead acetate from drinking water. Oxidative stress markers (advanced protein oxidation products, and malondialdehyde), antioxidant markers (total glutathione, reduced (GSH) to oxidized (GSSG) glutathione ratio, ferric ion reducing power, catalase, and paraoxonase-1), and in ammatory markers (hepatic nuclear factor-kβ expression, interleukin 1β level, and myeloperoxidase activity) in sera and liver homogenates were determined. Further, Biochemical liver function indicators (Alanine transaminase, aspartate transaminase, alkaline phosphatase, gamma-glutamyl transpeptidase, total bilirubin, total protein, albumin, and globulins) were quanti ed. Pb-induced liver damage was assessed with Histopathological observation.Results: B3 corrected lead-persuaded biochemical and histopathological changes in the rat's liver. In addition, treatment diminished Pb, oxidative stress, and in ammatory markers in the sera and liver homogenates of N-B3 and Pbt-B3 groups as well as elevated antioxidant markers (p < 0.001). ConclusionsNicotinamide through a decrease in Pb, oxidative stress, and in ammation prevented Pb prompted liver histopathological alternations and reduced liver dysfunction parameters.