Astragaloside IV Protects Against Oxidative Stress in Calf Small Intestine Epithelial Cells via NFE2L2-Antioxidant Response Element Signaling
Astragaloside IV Protects Against Oxidative Stress in Calf Small Intestine Epithelial Cells via NFE2L2-Antioxidant Response Element Signaling
复制标题
黄芪甲苷 IV 通过 NFE2L2 抗氧化反应元件信号传导保护小牛小肠上皮细胞免受氧化应激
DOI：
10.3390/ijms20246131
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发表时间：
2019-12-01
影响因子：
5.6
通讯作者：
Song, Enliang
中科院分区：
文献类型：
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作者：
Wang, Yafang;Jiang, Fugui;Song, Enliang
氧化应激可破坏肠上皮细胞的完整性和功能，引起胃肠道疾病。黄芪甲苷（ASIV）具有多种生物学和药理学特性，包括抗炎和抗氧化作用。本研究旨在探讨过氧化氢（H2O2）诱导的氧化应激对犊牛小肠上皮细胞的保护作用及其机制。asv预处理不仅可以提高细胞存活率，还可以减少活性氧的产生和凋亡，提高超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶的水平，减少丙二醛的形成。此外，asv预处理提高了核因子红系2相关因子2 （NFE2L2）、血红素加氧酶-1 （HMOX1）和NAD(P)H醌脱氢酶1 （NQO1）的mRNA和蛋白水平。NFE2L2抑制剂ML385先抑制NFE2L2的表达，然后阻断HMOX1和NQO1的表达。这些结果表明，asv处理通过激活nfe2l2 -抗氧化反应元件信号通路，有效地保护犊牛小肠上皮细胞免受h2o2诱导的氧化损伤。
Oxidative stress can damage intestinal epithelial cell integrity and function, causing gastrointestinal disorders. Astragaloside IV (ASIV) exhibits a variety of biological and pharmacological properties, including anti-inflammatory and antioxidant effects. The purpose of this research was to investigate the cytoprotective action of ASIV and its mechanisms in calf small intestine epithelial cells with hydrogen peroxide (H2O2)-induced oxidative stress. ASIV pretreatment not only increased cell survival, but it also decreased reactive oxygen species generation and apoptosis, enhanced superoxide dismutase, catalase, and glutathione peroxidase levels, and it reduced malondialdehyde formation. Furthermore, pretreatment with ASIV elevated the mRNA and protein levels of nuclear factor erythroid 2-related factor 2 (NFE2L2), heme oxygenase-1 (HMOX1), and NAD(P)H quinone dehydrogenase 1 (NQO1). The NFE2L2 inhibitor ML385 inhibited NFE2L2 expression and then blocked HMOX1 and NQO1 expression. These results demonstrate that ASIV treatment effectively protects against H2O2-induced oxidative damage in calf small intestine epithelial cells through the activation of the NFE2L2-antioxidant response element signaling pathway.