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亚硝酸钠诱导肝损伤中鱼肝油的作用:它有潜在保护作用吗?

Cod liver oil in sodium nitrite induced hepatic injury: does it have a potential protective effect?

作者信息

Sherif I O, Al-Gayyar M M

出版信息

Redox Rep. 2015 Jan;20(1):11-6. doi: 10.1179/1351000214Y.0000000097. Epub 2014 Jun 19.

DOI:10.1179/1351000214Y.0000000097
PMID:24945989
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6837344/
Abstract

OBJECTIVES

Exposure to sodium nitrites, a food additive, at high levels has been reported to produce reactive nitrogen and oxygen species that cause dysregulation of inflammatory responses and tissue injury. In this work, we examined the impact of dietary cod liver oil on sodium nitrite-induced inflammation in rats.

METHODS

Thirty-two adult male Sprague-Dawely rats were treated with 80 mg/kg sodium nitrite in presence/absence of 5 ml/kg cod liver oil. Liver sections were stained with hematoxylin/eosin. We measured hepatic tumor necrosis factor (TNF)-α, interleukin-1 beta (IL)-1β, C-reactive protein (CRP), transforming growth factor (TGF)-β1, and caspase-3.

RESULTS

Cod liver oil reduced sodium nitrite-induced hepatocyte damage. In addition, cod liver oil results in reduction of hepatic TNF-α, IL-1β, CRP, TGF-β1, and caspase-3 when compared with the sodium nitrite group.

DISCUSSION

Cod liver oil ameliorates sodium nitrite-induced hepatic injury via multiple mechanisms including blocking sodium nitrite-induced elevation of inflammatory cytokines, fibrosis mediators, and apoptosis markers.

摘要

目的

据报道,高剂量接触作为食品添加剂的亚硝酸钠会产生活性氮和氧物种,导致炎症反应失调和组织损伤。在本研究中,我们检测了膳食鱼肝油对亚硝酸钠诱导的大鼠炎症的影响。

方法

32只成年雄性Sprague-Dawely大鼠在有/无5 ml/kg鱼肝油的情况下接受80 mg/kg亚硝酸钠处理。肝脏切片用苏木精/伊红染色。我们测量了肝脏肿瘤坏死因子(TNF)-α、白细胞介素-1β(IL)-1β、C反应蛋白(CRP)、转化生长因子(TGF)-β1和半胱天冬酶-3。

结果

鱼肝油减轻了亚硝酸钠诱导的肝细胞损伤。此外,与亚硝酸钠组相比,鱼肝油使肝脏TNF-α、IL-1β、CRP、TGF-β1和半胱天冬酶-3水平降低。

讨论

鱼肝油通过多种机制改善亚硝酸钠诱导的肝损伤,包括阻止亚硝酸钠诱导的炎性细胞因子、纤维化介质和凋亡标志物的升高。

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Eur Cytokine Netw. 2013 Jul-Sep;24(3):114-21. doi: 10.1684/ecn.2013.0341.
2
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Pharm Biol. 2013 Nov;51(11):1435-43. doi: 10.3109/13880209.2013.796564. Epub 2013 Jul 18.
3
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Nutr J. 2013 Jul 15;12:98. doi: 10.1186/1475-2891-12-98.
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