Nigella sativa oil attenuates chronic nephrotoxicity induced by oral sodium nitrite: Effects on tissue fibrosis and apoptosis

被引:33
作者
Al-Gayyar, Mohammed M. H. [1 ,2 ]
Hassan, Hanan M. [3 ]
Alyoussef, Abdullah [4 ]
Abbas, Ahmed [5 ]
Darweish, Mohamed M. [1 ]
El-Hawwary, Amany A. [6 ]
机构
[1] Univ Tabuk, Dept Pharmaceut Chem, Fac Pharm, Tabuk, Saudi Arabia
[2] Univ Mansoura, Dept Clin Biochem, Fac Pharm, Mansoura, Egypt
[3] Princess Noura Bint Abulrahman Univ, Dept Pharmaceut Sci, Coll Pharm, Riyadh 11671, Saudi Arabia
[4] Univ Tabuk, Dept Internal Med, Fac Med, Tabuk, Saudi Arabia
[5] Univ Mansoura, Dept Pharmacognosy, Fac Pharm, Mansoura, Egypt
[6] Univ Mansoura, Dept Histol & Cell Biol, Fac Med, Mansoura, Egypt
关键词
Black cumin; CRP; Cytochrome C oxidase; Glycogen; MCP-1; TGF-beta1; CYTOCHROME-C-OXIDASE; COD-LIVER OIL; OXIDATIVE STRESS; AQUEOUS EXTRACT; RATS; THYMOQUINONE; TOXICITY; SEEDS; NITRATE; ANTIOXIDANT;
D O I
10.1179/1351000215Y.0000000035
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:50 / 60
页数:11
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