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Published on: May 4, 2020
Astragalus polysaccharides mediated preventive effects on bronchopulmonary dysplasia in rats
Xiao-Hong Wang1, Hong-Ling Jia2, Li Deng3
1Department of Neonatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Insights
Astragalus polysaccharides (APS) show protective effects against bronchopulmonary dysplasia (BPD) in neonatal rats. APS reduces inflammation and oxidative stress, mitigating lung damage in a BPD model.
Area of Science:
- Neonatal Medicine
- Pharmacology
- Pulmonology
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease affecting premature infants.
- Investigating Astragalus polysaccharides (APS) for BPD prevention is crucial.
Purpose of the Study:
- To evaluate the preventive effects of Astragalus polysaccharides (APS) on bronchopulmonary dysplasia (BPD).
- To explore the underlying molecular mechanisms of APS in mitigating BPD.
Main Methods:
- Newborn Sprague-Dawley rats were used to model BPD.
- Lung tissues were analyzed for pathomorphology, oxidative stress markers (SOD, MDA), and inflammatory markers (NF-κBp65, CD31, ICAM-1, TNF-α) via protein and mRNA expression.
Main Results:
- APS treatment reduced inflammatory cell infiltration compared to the BPD model.
- APS increased superoxide dismutase (SOD) activity and decreased malondialdehyde (MDA) levels.
- APS modulated inflammatory mediators, decreasing NF-κBp65, ICAM-1, and TNF-α, while increasing CD31 expression.
Conclusions:
- Astragalus polysaccharides (APS) demonstrate protective effects against BPD in neonatal rats.
- APS reduces airway remodeling and alveolar damage through anti-inflammatory and antioxidant mechanisms.
Background:
Bronchopulmonary dysplasia (BPD) is a multifactor chronic lung disease that mainly affects premature infants. In this study, we investigate the preventive effects of Astragalus polysaccharides (APS) on BPD, and explore its potential molecular mechanisms.
Methods:
Lung tissues of newborn Sprague-Dawley rats from the control group, the room air plus low-dose APS group, the room air plus high-dose APS group, the BPD model group, the low-dose APS group (20 mg/kg d), and the high-dose APS group (40 mg/kg d) were examined at the 4th, 10th, and 14th d of life. The pathomorphological change was evaluated by hematoxylin-eosin staining. The content levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by the assay kit. Moreover, the protein and/or mRNA expression levels of NF-κBp65, CD31, ICAM-1, and TNF-α were also detected by corresponding methods.
Results:
APS decreased the inflammatory cells infiltrating compared with the BPD group. For the APS group, the activity of SOD was increased and the content of MDA was reduced compared with the BPD group at any time point. The protein and mRNA expression levels of NF-κBp65, ICAM-1, and TNF-α were all decreased, while the protein expression level of CD31 was increased in the APS-treated group, with the most significant difference of the high-dose group (P < 0.01) compared with the BPD group after birth on the 4th, 10th, and 14th d.
Conclusion:
APS can reduce airway remodeling and alveolar damage by its modulation of inflammatory mediators and antioxidation, suggesting some protective effects on BPD of neonatal rats.
