اثر حفاظت کبدی نیکوتینامید برابر سمیت کبدی ناشی از سرب در موشهایی صحرایی بااصلاح مسیر پیامرسانی کاپا-بی و متابولیسم گلوتاتیون

عنوان انگليسی

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

خلاصه انگلیسی

Lead (Pb) poisoning is one of the pivotal environmental issues and prompts liver dysfunction by elevating oxidative stress and infammation. Nicotinamide (NA) defciency enhances sensitivity to Pb toxicity. So, we investigated the efect of nicotinamide (NA) on the rat’s liver histopathological and biochemical profles in a rat model of Pb toxicity. Thirty-six rats were divided into four groups (nine rats at each): normal (N), lead toxicity (Pbt), and NA-treated N and Pbt groups. Treated groups took NA (180 mg/L in drinking water for one month). Pb intoxication was motivated in rats by acquiring 50 mg/L lead acetate in drinking water. Oxidative stress markers (advanced oxidation protein products and malondialdehyde), antioxidant markers (total glutathione, reduced glutathione to oxidized glutathione ratio, ferric ion reducing power, catalase, and paraoxonase-1), and infammatory markers (hepatic nuclear factor-kβ expression, interleukin 1β level, and myeloperoxidase activity) in sera and liver homogenates were determined. In addition, the biochemical parameters of the liver function were measured. Finally, the liver of rats was evaluated by histopathological observation. NA corrected lead-persuaded biochemical and histopathological changes in the rat’s liver. In addition, treatment decreased Pb, oxidative stress, and infammatory markers in the sera and liver homogenates of N and Pbt groups. In addition, it elevated antioxidant markers (p < 0.001). NA prevented Pb-induced liver histopathological alternations and reduced liver dysfunction by reducing Pb, oxidative stress, and infammation. Moreover, raising GSH/GSSG and diminishing the hepatic NF-kβ pathway are cardinal mechanisms of the treatment against Pb-motivated hepatotoxicity in rats.

Document Downloads