Abstract
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.
Highlights
The intestinal mucosa is one of the main points of contact between the body and the external environment [1]
Viability was significantly lower after treatment with 350 μM H2O2, which caused an approximately 59% loss in cell viability; where this concentration was used in subsequent experiments
The intestinal mucosa is one of the main barriers between the body and the external environment, and it functions by selectively absorbing nutrients and preventing invasion from the external environment
Summary
The intestinal mucosa is one of the main points of contact between the body and the external environment [1]. Small intestinal epithelial cells are the first physiological line of defense in the mucosa, which selectively absorbs nutrients and protects against pathogenic invasions from the external environment [2]. Oxidative stress, arising from the excessive generation of reactive oxygen species (ROS) and imbalances in the antioxidant system, can damage multiple cellular components through DNA hydroxylation, protein denaturation, lipid peroxidation, and membrane rupture. This outcome leads to apoptosis and other modes of cell death [4,5].
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