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芹菜素对小鼠呋喃诱导毒性的保护作用。

Protective effects of apigenin against furan-induced toxicity in mice.

作者信息

Wang Enting, Chen Fang, Hu Xiaosong, Yuan Yuan

机构信息

College of Quartermaster Technology, Jilin University, Changchun, China130062.

出版信息

Food Funct. 2014 Aug;5(8):1804-12. doi: 10.1039/c4fo00038b.

Abstract

Furan, a food contaminant formed by heating, is possibly carcinogenic to humans. In this study, we discussed the effect of administration of apigenin on furan-induced toxicity by determining the ROS content, oxidative damage, cytokine levels, DNA damage, and the liver and kidney damage in a mouse model. Our data showed that apigenin administered at 5, 10, and 20 mg kg(-1) bw per day could decrease the toxicity induced by furan to different extents. On one hand, apigenin has the ability to increase the oxidative damage indexes of glutathione (GSH) and glutathione-S-transferase (GST) as well as superoxide dismutase (SOD) activities but decrease myeloperoxidase (MPO) activities and maleic dialdehyde (MDA) content in the liver and kidney of mice treated with furan. On the other hand, it could decrease cytokine levels of tumor necrosis factor α (TNF-α), interleukin (IL)-1β, and interleukin (IL)-6 but increase interleukin (IL)-10 in the serum of furan-treated mice. At the same time, the three concentrations of apigenin elected in this paper all could decrease the ROS content, DNA damage index of 8-hydroxy-desoxyguanosine (8-OHdG), the liver and kidney damage indexes of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactic dehydrogenase (LDH), and blood urea nitrogen (BUN) and creatinine content in furan-treated mice to different extents. The protective effects of apigenin against furan-induced toxicity damage were mainly due to its excellent ability to scavenge free radicals and inhibit lipid oxidation. This is important when considering the use of apigenin as a dietary supplement for beneficial chemoprevention of furan toxicity.

摘要

呋喃是一种加热产生的食品污染物,可能对人类具有致癌性。在本研究中,我们通过测定小鼠模型中的活性氧含量、氧化损伤、细胞因子水平、DNA损伤以及肝和肾损伤,探讨了芹菜素给药对呋喃诱导毒性的影响。我们的数据表明,每天以5、10和20 mg kg(-1)体重的剂量给予芹菜素可在不同程度上降低呋喃诱导的毒性。一方面,芹菜素能够提高谷胱甘肽(GSH)、谷胱甘肽-S-转移酶(GST)的氧化损伤指标以及超氧化物歧化酶(SOD)活性,但降低用呋喃处理的小鼠肝脏和肾脏中的髓过氧化物酶(MPO)活性和丙二醛(MDA)含量。另一方面,它可以降低呋喃处理小鼠血清中肿瘤坏死因子α(TNF-α)、白细胞介素(IL)-1β和白细胞介素(IL)-6的细胞因子水平,但增加白细胞介素(IL)-10。同时,本文选择的三种芹菜素浓度均能不同程度地降低呋喃处理小鼠的活性氧含量、8-羟基脱氧鸟苷(8-OHdG)的DNA损伤指数、天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)和乳酸脱氢酶(LDH)的肝和肾损伤指数以及血尿素氮(BUN)和肌酐含量。芹菜素对呋喃诱导的毒性损伤的保护作用主要归因于其出色的清除自由基和抑制脂质氧化的能力。在考虑将芹菜素用作预防呋喃毒性的有益化学预防的膳食补充剂时,这一点很重要。

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