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硫辛酸对肉鸡黄曲霉毒素B₁诱导的肝脏氧化损伤和炎症反应的保护作用的分子机制

Molecular Mechanisms of Lipoic Acid Protection against Aflatoxin B₁-Induced Liver Oxidative Damage and Inflammatory Responses in Broilers.

作者信息

Ma Qiugang, Li Yan, Fan Yu, Zhao Lihong, Wei Hua, Ji Cheng, Zhang Jianyun

机构信息

State Key Laboratory of Animal Nutrition, College of Animal Science and Technology, China Agricultural University, Beijing 100193, China.

Translational Medicine Lab, Chinese National Human Genome Center, Beijing 100176, China.

出版信息

Toxins (Basel). 2015 Dec 14;7(12):5435-47. doi: 10.3390/toxins7124879.

Abstract

Alpha-lipoic acid (α-LA) was evaluated in this study for its molecular mechanisms against liver oxidative damage and inflammatory responses induced by aflatoxin B₁ (AFB₁). Birds were randomly allocated into four groups with different diets for three weeks: a basal diet, a 300 mg/kg α-LA supplementation in a basal diet, a diet containing 74 μg/kg AFB₁, and 300 mg/kg α-LA supplementation in a diet containing 74 μg/kg AFB₁. In the AFB₁ group, the expression of GSH-PX mRNA was down-regulated (p < 0.05), and the levels of lipid peroxide and nitric oxide were increased (p < 0.05) in the chicken livers compared to those of the control group. Additionally, the mRNA level of the pro-inflammatory factor interleukin-6 was up-regulated significantly (p < 0.05), the protein expressions of both the nuclear factor kappa B (NF-κB) p65 and the inducible nitric oxide synthase were enhanced significantly (p < 0.05) in the AFB₁ group. All of these negative effects were inhibited by α-LA. These results indicate that α-LA may be effective in preventing hepatic oxidative stress, down-regulating the expression of hepatic pro-inflammatory cytokines, as well as inhibiting NF-κB expression.

摘要

本研究评估了α-硫辛酸(α-LA)对抗黄曲霉毒素B₁(AFB₁)诱导的肝脏氧化损伤和炎症反应的分子机制。将鸡随机分为四组,给予不同饮食,持续三周:基础饮食组、基础饮食中添加300 mg/kg α-LA的组、含74 μg/kg AFB₁的饮食组以及含74 μg/kg AFB₁的饮食中添加300 mg/kg α-LA的组。在AFB₁组中,与对照组相比,鸡肝脏中谷胱甘肽过氧化物酶(GSH-PX)mRNA的表达下调(p < 0.05),脂质过氧化物和一氧化氮水平升高(p < 0.05)。此外,促炎因子白细胞介素-6的mRNA水平显著上调(p < 0.05),AFB₁组中核因子κB(NF-κB)p65和诱导型一氧化氮合酶的蛋白表达均显著增强(p < 0.05)。所有这些负面影响均被α-LA抑制。这些结果表明,α-LA可能有效预防肝脏氧化应激,下调肝脏促炎细胞因子的表达,并抑制NF-κB表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4565/4690129/e8a5dbb1f0e5/toxins-07-04879-g001.jpg

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