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Ginkgolide B Alleviates Airway Inflammation in Hyperoxia Lung Injury
Xuesong Wang1, Mingwu Chen1, Yong Lv1
1Department of Pediatrics, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Insights
Platelet-activating factor (PAF) drives lung inflammation in bronchopulmonary dysplasia (BPD). Ginkgolide B (GB) inhibits PAF-activated neutrophils, reducing lung damage in a neonatal rat model, suggesting a potential therapy for BPD.
Area of Science:
- Neonatal research
- Pulmonology
- Inflammation research
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in preterm infants, often involving inflammation due to prolonged hyperoxia.
- Platelet-activating factor (PAF) is a known inflammatory mediator, but its specific role in BPD pathogenesis remains unclear.
- This study investigates Ginkgolide B (GB), a PAF receptor antagonist, as a potential therapeutic agent for hyperoxia-induced lung injury.
Purpose of the Study:
- To investigate the role of Platelet-Activating Factor (PAF) in neonatal lung inflammation associated with Bronchopulmonary Dysplasia (BPD).
- To evaluate the therapeutic efficacy of Ginkgolide B (GB), a PAF receptor antagonist, in mitigating hyperoxia-induced lung injury.
- To explore the mechanisms by which PAF contributes to neutrophil activation and lung damage in a BPD model.
Main Methods:
- Observed platelet and neutrophil activation markers in bronchoalveolar lavage fluid (BALF) from BPD patients.
- Measured PAF levels in peripheral blood and BALF, and analyzed BALF supernatant for inflammatory cytokines.
- Stimulated neutrophils in vitro with PAF to assess inflammatory gene expression.
- Utilized a neonatal rat model of hyperoxia-induced lung injury, treating with Ginkgolide B (GB).
Main Results:
- BPD patients exhibited early platelet and neutrophil activation, with elevated PAF and myeloperoxidase-DNA (MPO-DNA) in plasma.
- PAF stimulation in vitro upregulated IL-6 mRNA in neutrophils and altered CD62L expression.
- BALF from BPD infants showed increased levels of PAF, IL-6, IL-8, and GM-CSF.
- GB treatment significantly reduced lung damage in hyperoxia-exposed rats, decreasing neutrophil-derived IL-6 and inhibiting the IL-6/Jak2/Stat3 signaling pathway.
Conclusions:
- PAF activation of neutrophils contributes to lung inflammation and damage in Bronchopulmonary Dysplasia (BPD).
- Ginkgolide B (GB) effectively inhibits PAF-induced neutrophil activation and IL-6 production, thereby alleviating lung injury.
- Targeting the PAF pathway with Ginkgolide B (GB) presents a promising therapeutic strategy for BPD and other hyperoxia-related lung diseases.
Background:
Bronchopulmonary dysplasia (BPD) is a chronic lung disease characterized by inflammation, often caused by prolonged hyperoxia exposure in preterm infants. Platelet-activating factor (PAF) is a potent inflammatory mediator, but its role in BPD is unclear. This study explores the therapeutic potential of the PAF receptor antagonist Ginkgolide B (GB) in hyperoxia-induced lung injury.
Methods:
We observed the activation status of platelets and neutrophils in BALF（bronchoalveolar lavage fluid) of patients with BPD. The supernatant of BALF from patients was sent for protein chip detection and validated by ELISA. We also measured the levels of PAF in peripheral blood and BALF. In vitro experiments, we stimulated neutrophils with PAF to detect the expression of inflammatory cytokine genes. Finally, we established a neonatal rat model of hyperoxia-induced lung injury mimicking BPD and intervened with GB.
Results:
We observed early activation of platelets and neutrophils in the peripheral blood of BPD patients, with elevated plasma levels of PAF and myeloperoxidase-DNA (MPO-DNA). In BALF, neutrophils showed increased CD66b and MPO expression. In vitro, PAF stimulation decreased CD62L expression on neutrophils and upregulated IL-6 mRNA. Elevated levels of PAF, IL-6, IL-8, and GM-CSF were found in BPD infants' BALF supernatant. Using animal models of BPD, we found that GB significantly reduced lung damage in hyperoxia-exposed rats. GB decreased neutrophil-derived IL-6 and downregulated key proteins in the IL-6 signaling pathway (pJak2 and pStat3).
Conclusion:
Our study demonstrates that PAF activates neutrophils and promotes their lung residence. GB effectively inhibits neutrophil-derived IL-6 and alleviates hyperoxia-induced lung damage. Targeting the PAF pathway with GB may be a promising strategy for BPD and other hyperoxia-related lung diseases.
