Mohammed M H Al-Gayyar1,2, Hanan M Hassan3, Abdullah Alyoussef4, Ahmed Abbas5, Mohamed M Darweish1, Amany A El-Hawwary6. 1. a Department of Pharmaceutical Chemistry, Faculty of Pharmacy , University of Tabuk , Saudi Arabia. 2. b Department of Clinical Biochemistry, Faculty of Pharmacy , University of Mansoura , Egypt. 3. c Department of Pharmaceutical Sciences, College of Pharmacy , Princess Noura bint Abulrahman University , Riyadh 11671 , KSA. 4. d Department of Internal Medicine, Faculty of Medicine , University of Tabuk , Saudi Arabia. 5. e Department of Pharmacognosy, Faculty of Pharmacy , University of Mansoura , Egypt. 6. f Department of Histology and Cell Biology, Faculty of Medicine , University of Mansoura , Egypt.
Abstract
OBJECTIVES: Sodium nitrite, a food preservative, has been reported to increase oxidative stress indicators such as lipid peroxidation, which can affect different organs including the kidney. Here, we investigated the toxic effects of oral sodium nitrite on kidney function in rats and evaluated potential protective effects of Nigella sativa oil (NSO). METHODS: Seventy adult male Sprague-Dawley rats received 80 mg/kg sodium nitrite orally in the presence or absence of NSO (2.5, 5, and 10 ml/kg) for 12 weeks. Morphological changes were assessed by hematoxylin and eosin, Mallory trichome, and periodic acid-Schiff staining. Renal tissues were used for measurements of oxidative stress markers, C-reactive protein, cytochrome C oxidase, transforming growth factor (TGF)-beta1, monocyte chemotactic protein (MCP)-1, pJNK/JNK, and caspase-3. RESULTS: NSO significantly reduced sodium nitrite-induced elevation in serum urea and creatinine, as well as increasing normal appearance of renal tissue. NSO also prevented reductions in glycogen levels caused by sodium nitrite alone. Moreover, NSO treatment resulted in dose-dependent significant reductions in fibrosis markers after sodium nitrite-induced 3- and 2.7-fold increase in MCP-1 and TGF-beta1, respectively. Finally, NSO partially reduced the elevated caspase-3 and pJNK/JNK. DISCUSSION: NSO ameliorates sodium nitrite-induced nephrotoxicity through blocking oxidative stress, attenuation of fibrosis/inflammation, restoration of glycogen level, amelioration of cytochrome C oxidase, and inhibition of apoptosis.
OBJECTIVES:Sodium nitrite, a food preservative, has been reported to increase oxidative stress indicators such as lipid peroxidation, which can affect different organs including the kidney. Here, we investigated the toxic effects of oral sodium nitrite on kidney function in rats and evaluated potential protective effects of Nigella sativa oil (NSO). METHODS: Seventy adult male Sprague-Dawley rats received 80 mg/kg sodium nitrite orally in the presence or absence of NSO (2.5, 5, and 10 ml/kg) for 12 weeks. Morphological changes were assessed by hematoxylin and eosin, Mallory trichome, and periodic acid-Schiff staining. Renal tissues were used for measurements of oxidative stress markers, C-reactive protein, cytochrome C oxidase, transforming growth factor (TGF)-beta1, monocyte chemotactic protein (MCP)-1, pJNK/JNK, and caspase-3. RESULTS:NSO significantly reduced sodium nitrite-induced elevation in serum urea and creatinine, as well as increasing normal appearance of renal tissue. NSO also prevented reductions in glycogen levels caused by sodium nitrite alone. Moreover, NSO treatment resulted in dose-dependent significant reductions in fibrosis markers after sodium nitrite-induced 3- and 2.7-fold increase in MCP-1 and TGF-beta1, respectively. Finally, NSO partially reduced the elevated caspase-3 and pJNK/JNK. DISCUSSION: NSO ameliorates sodium nitrite-induced nephrotoxicity through blocking oxidative stress, attenuation of fibrosis/inflammation, restoration of glycogen level, amelioration of cytochrome C oxidase, and inhibition of apoptosis.
Entities:
Keywords:
Black cumin; CRP; Cytochrome C oxidase; Glycogen; MCP-1; TGF-beta1
Authors: Everson A Nunes; Luiz M Gonçalves-Neto; Francielle B D Ferreira; Cristiane dos Santos; Luiz C Fernandes; Antonio C Boschero; Philip C Calder; Alex Rafacho Journal: Appl Physiol Nutr Metab Date: 2013-06-17 Impact factor: 2.665