Affiliation:
1. Department of Preventive Medicine, School of Public Health, Hengyang Medical School, University of South China , 28 West Changsheng Road, Hengyang, 421001 , China
Abstract
Abstract
Background
The protective effects of astragaloside IV (ASIV) on various diseases are well known, but its potential impact on radiation-induced bystander effect (RIBE) has remained unclear.
Objective
This study aimed to explore the protective mechanism of ASIV against oxidative damage caused by RIBE in LO2 cells.
Methods
To construct the RIBE model, the conditioned medium from HepG2 cells irradiated with radiation was transferred to nonirradiated LO2 cells. LY294002, a commonly used phosphatidylinositol 3-kinase/Akt pathway inhibitor, was added to LO2 cells 1 h before exposing HepG2 cells to radiation. LO2 cells were then collected for analyses after RIBE exposure.
Results
The study found that ASIV significantly improved cell proliferation and promoted the recovery of mitochondrial membrane potential while reducing the rate of apoptosis. Western blot analyses demonstrated that ASIV upregulated B-cell lymphoma 2 and downregulated B-cell lymphoma 2-related X protein and cleaved-caspase 3. Measurement of reactive oxygen species, superoxide dismutase, glutathione peroxidase, and malondialdehyde levels showed that ASIV effectively restored the oxidative stress state induced by RIBE. Additionally, immunofluorescence and western blots analyses confirmed that ASIV enhanced the translocation of Nrf2 to the nucleus and activated downstream nicotinamide adenine dinucleotide phosphate: quinine oxidoreductase 1 and heme oxygenase 1. Importantly, Akt pathway inhibitor repressed ASIV-induced activation of Nrf2 and its protective effect against RIBE.
Conclusion
This study demonstrates that ASIV protects LO2 cells against oxidative damage caused by RIBE through activation of the Akt/Nrf2 pathway.
Funder
Natural Science Foundation of Hunan Province
Health Commission Scientific Research Project of Hunan Province
Scientific Research Project of Education Bureau of Hunan Province
National Natural Science Foundation of China
Publisher
Oxford University Press (OUP)
Subject
Health, Toxicology and Mutagenesis,Toxicology
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