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维生素 E 可减轻对硫磷诱导的大鼠肠道氧化应激、屏障功能和形态变化的毒性作用。

Vitamin E alleviates phoxim-induced toxic effects on intestinal oxidative stress, barrier function, and morphological changes in rats.

机构信息

Institute of Animal Nutrition, Northeast Agricultural University, Harbin, 150030, People's Republic of China.

出版信息

Environ Sci Pollut Res Int. 2018 Sep;25(26):26682-26692. doi: 10.1007/s11356-018-2666-y. Epub 2018 Jul 12.

DOI:10.1007/s11356-018-2666-y
PMID:30003487
Abstract

Phoxim is an organic phosphorus pesticide that remains easily in the environment, such as human food and animal feed. The objective of this study was to explore the effect of vitamin E on phoxim-induced oxidative stress in the intestinal tissues of Sprague-Dawley (SD) rats. Forty-eight Sprague-Dawley rats were randomly assigned to a control group and three treatment groups: treatment group 1 (phoxim: 20 mg/kg·BW), treatment group 2 (phoxim: 180 mg/kg·BW), and treatment 3 (vitamin E + phoxim: 200 mg/kg·BW + 180 mg/kg·BW). Phoxim was given by gavage administration once a day for 28 days. The results showed that phoxim significantly reduced jejunum villus height in rats (P < 0.05), and decreased the mRNA expression of junction protein genes of rats, including Occlidin and Claudin-4 (P < 0.05). Phoxim reduced GSH content and T-AOC level in the intestinal mucosa (P < 0.05). The mRNA expression levels of oxidative stress-related genes (Nrf2 and GPx2) were decreased. The mRNA expression of SOD was significantly increased. In addition, phoxim increased the level of interleukin-6 (IL-6) in jejunum mucosa and significantly reduced the level of IL-8 in ileum mucosas, while significantly increased TNF-α secretion. The mRNA expression levels of IL-1β, IL-6, and IL-8 were significantly decreased, and mRNA expression of TNF-α was significantly increased (P < 0.05). Phoxim also increased the DNA expression of total cecal bacteria and Escherichia coli, inhibited the DNA expression of Lactobacillus and destroyed the intestinal barrier. Two hundred milligrams per kilogram BW vitamin E reduced the effect of phoxim on intestinal structure, alleviated the oxidative stress in intestinal tissue, and decreased the level of TNF-α. The mRNA expressions of antioxidative stress genes (SOD and GPx2) were significantly increased. The DNA expression level of Lactobacillus was significantly increased. In conclusion, vitamin E helped reduce the toxicity of organophosphate pesticides, such as phoxim on rat intestinal tissue.

摘要

辛硫磷是一种有机磷农药,在人类食物和动物饲料等环境中容易残留。本研究旨在探讨维生素 E 对辛硫磷诱导的 Sprague-Dawley(SD)大鼠肠组织氧化应激的影响。将 48 只 Sprague-Dawley 大鼠随机分为对照组和 3 个处理组:处理组 1(辛硫磷:20mg/kg·BW)、处理组 2(辛硫磷:180mg/kg·BW)和处理 3(维生素 E+辛硫磷:200mg/kg·BW+180mg/kg·BW)。辛硫磷每天灌胃给药 1 次,共 28 天。结果显示,辛硫磷显著降低了大鼠空肠绒毛高度(P<0.05),降低了大鼠紧密连接蛋白基因 Occlidin 和 Claudin-4 的 mRNA 表达(P<0.05)。辛硫磷降低了肠黏膜中 GSH 含量和 T-AOC 水平(P<0.05)。氧化应激相关基因(Nrf2 和 GPx2)的 mRNA 表达水平降低,SOD 的 mRNA 表达水平显著增加。此外,辛硫磷增加了空肠黏膜中白细胞介素-6(IL-6)的水平,显著降低了回肠黏膜中白细胞介素-8(IL-8)的水平,同时显著增加了 TNF-α 的分泌。IL-1β、IL-6 和 IL-8 的 mRNA 表达水平显著降低,TNF-α 的 mRNA 表达水平显著增加(P<0.05)。辛硫磷还增加了总盲肠细菌和大肠杆菌的 DNA 表达,抑制了乳酸菌的 DNA 表达,破坏了肠道屏障。200mg/kg BW 维生素 E 降低了辛硫磷对肠道结构的影响,缓解了肠组织的氧化应激,降低了 TNF-α 的水平。抗氧化应激基因(SOD 和 GPx2)的 mRNA 表达显著增加。乳酸菌的 DNA 表达水平显著增加。综上所述,维生素 E 有助于减轻辛硫磷等有机磷农药对大鼠肠组织的毒性。

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