Astragaloside IV Protects Against Oxidative Stress in Calf Small Intestine Epithelial Cells via NFE2L2-Antioxidant Response Element Signaling
文献类型: 外文期刊
作者: Wang, Yafang 1 ; Jiang, Fugui 1 ; Cheng, Haijian 1 ; Tan, Xiuwen 1 ; Liu, Yifan 1 ; Wei, Chen 1 ; Song, Enliang 1 ;
作者机构: 1.Shandong Acad Agr Sci, Inst Anim Sci & Vet Med, Sangyuan Rd 8, Jinan 250100, Peoples R China
2.Shandong Key Lab Anim Dis Control & Breeding, Sangyuan Rd 8, Jinan 250100, Peoples R China
3.Shandong Normal Univ, Coll Life Sci, East Wenhua Rd 88, Jinan 250014, Peoples R China
关键词: Astragaloside IV; small intestine epithelial cells; oxidative stress; hydrogen peroxide; nuclear factor erythroid 2-related factor 2; calf
期刊名称:INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES ( 影响因子:5.923; 五年影响因子:6.132 )
ISSN:
年卷期: 2019 年 20 卷 24 期
页码:
收录情况: SCI
摘要: 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.
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