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黄芪多糖通过活性氧(ROS)途径保护鸡胚成纤维细胞对抗镉诱导的自噬损伤。

Astragalus Polysaccharide Protects Against Cadmium-Induced Autophagy Injury Through Reactive Oxygen Species (ROS) Pathway in Chicken Embryo Fibroblast.

机构信息

College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.

Key Laboratory of the Provincial Education Department of Heilongjiang, for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin, 150030, China.

出版信息

Biol Trace Elem Res. 2022 Jan;200(1):318-329. doi: 10.1007/s12011-021-02628-y. Epub 2021 Mar 11.

Abstract

Cadmium (Cd) is a harmful heavy metal pollutant, which can cause oxidative stress in the body and induce cell damage. Reactive oxygen species (ROS) is a general term for substances that contain oxygen and are active in the body. However, excessive ROS can damage the body. Cadmium poisoning can cause a large amount of ROS in cells and autophagy. Astragalus polysaccharide (APS) is a plant polysaccharide with biological functions, such as antioxidant and anti-stress activities. In this study, chicken embryo fibroblasts (CEF) were used to determine the relationship between ROS and autophagy damage of Cd-infected cells and the mechanism of APS on cadmium-induced autophagy damage. The results showed that a 10-μL dose of 10 μmol/L cadmium chloride (CdCl) can induce CEF autophagy and damage when CEF was added for 36 h. Cadmium induced CEF autophagy damage by increasing ROS production. APS could significantly reduce ROS production and LC3-II and Beclin-1 protein expression, increase the expression of mTOR and the level of antioxidation, and restore the viability and morphological damage of CEF exposed to Cd. Our study suggests that APS can alleviate Cd-induced CEF autophagy damage by reducing the production of ROS.

摘要

镉(Cd)是一种有害的重金属污染物,它会在体内引起氧化应激,并诱导细胞损伤。活性氧(ROS)是指在体内具有活性并含有氧的物质的总称。然而,过量的 ROS 会对身体造成损害。镉中毒会导致细胞内产生大量的 ROS 和自噬。黄芪多糖(APS)是一种具有生物功能的植物多糖,如抗氧化和抗应激活性。在这项研究中,鸡胚成纤维细胞(CEF)被用来确定 ROS 与 Cd 感染细胞自噬损伤之间的关系,以及 APS 对镉诱导自噬损伤的作用机制。结果表明,当添加 10μL 剂量为 10μmol/L 的氯化镉(CdCl)时,CEF 会在 36 小时内发生自噬和损伤。镉通过增加 ROS 的产生诱导 CEF 自噬损伤。APS 可显著降低 ROS 的产生以及 LC3-II 和 Beclin-1 蛋白的表达,增加 mTOR 的表达和抗氧化水平,并恢复暴露于 Cd 的 CEF 的活力和形态损伤。我们的研究表明,APS 可以通过减少 ROS 的产生来减轻 Cd 诱导的 CEF 自噬损伤。

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