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Antioxidant and anti-inflammatory effects of Astragalus polysaccharide on EA.hy926 cells
Wei Min Huang1, Yong Qi Liang, Li Jun Tang
1Department of Neonatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Insights
Astragalus polysaccharide (APS) reduces oxidative stress and inflammation in a cell model of bronchopulmonary dysplasia (BPD). APS demonstrates antioxidant and anti-inflammatory effects, offering potential therapeutic benefits for BPD.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in preterm infants.
- Oxidative stress and inflammation are key contributors to BPD pathogenesis.
- Novel therapeutic strategies targeting these pathways are needed.
Purpose of the Study:
- To investigate the therapeutic potential of astragalus polysaccharide (APS) in a cellular model of BPD.
- To elucidate the antioxidant and anti-inflammatory mechanisms of APS in lung cells.
Main Methods:
- Established EA.hy926 cell model simulating BPD conditions (hyperoxia).
- Biochemical assays to measure superoxide dismutase (SOD), malondialdehyde (MDA), and reactive oxygen species (ROS).
- RT-PCR and Western blotting to assess inflammatory markers (IL-8, ICAM-1, NF-κB p65).
Main Results:
- APS treatment significantly reduced ROS and MDA levels.
- APS significantly increased SOD production, indicating antioxidant activity.
- APS downregulated the expression of IL-8, ICAM-1, and NF-κB p65, suggesting anti-inflammatory effects.
Conclusions:
- Astragalus polysaccharide exhibits significant antioxidant properties by enhancing SOD and inhibiting lipid peroxidation.
- APS effectively mitigates the inflammatory response implicated in BPD pathogenesis.
- These findings suggest APS as a potential therapeutic agent for preventing or treating BPD.
Abstract:
The aim of this study was to explore the role of astragalus polysaccharide (APS) in the pathogenesis of bronchopulmonary dysplasia (BPD) in preterm children using an established BPD cell model. EA.hy926 cell cultures were divided into three groups: the air group as the blank control, the hyperoxia group as the experimental control and the APS group (2.5 mg/ml). The production of superoxide dismutase (SOD), malondialdehyde (MDA) and reactive oxygen species (ROS) were analyzed by biochemical assays. Real-time reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used to detect the RNA and protein expression levels of inflammatory cytokines, including interleukin (IL)-8, intercellular adhesion molecule 1 (ICAM-1) and nuclear factor (NF)-κB p65. Compared with the hyperoxia group, the ROS and MDA levels of the APS group were significantly reduced. By contrast, SOD production was significantly increased. The expression of IL-8, ICAM-1 and NF-κB p65 in the APS group was downregulated. APS acts as an antioxidant by stimulating SOD production while inhibiting lipid peroxidation in the EA.hy926 cells. Furthermore, this study demonstrated that APS retards the inflammatory response, as shown by the reduced expression of NF-κB p65, IL-8 and ICAM-1 when APS was added.
