SEMA3A protects against hyperoxia-induced lung injury in a bronchopulmonary dysplasia model of newborn rat by inhibiting ERK pathway

Liang, Zhenyu; Zhang, Xiao; Liu, Yingxian; Wu, Qianmei; You, Chuming

doi:10.15586/aei.v49i6.478

Cited by 12 publications

(6 citation statements)

References 32 publications

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“…Hyperoxia is often administered to premature babies, and a long-term exposure to hyperoxia potentially induces oxygen toxicity, chronic lung injury, and bronchopulmonary dysplasia. 1 Bronchopulmonary dysplasia induces arrest of vascular and alveolar development, and refers to common cause of respiratory disease with leading mortality and morbidity rates. 2 Bronchopulmonary dysplasia is characterized by fibrosis, abnormal lung function, mesenchymal cell hyperplasia, pulmonary growth arrest, and enlarged alveoli.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of EDA2R alleviates hyperoxia-induced lung epithelial cell injury by inhibiting NF-κB pathway

Nan

Jia

Yang

et al. 2022

Allergol Immunopathol

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Background: Long-term hyperoxia impairs growth of the lungs and contributes to develop-ment of bronchopulmonary dysplasia. Ectodysplasin A (EDA) binds to ectodysplasin A2 receptor (EDA2R) and is essential for normal prenatal development. The functioning of EDA2R in bronchopulmonary dysplasia is investigated in this study. Methods: Murine lung epithelial cells (MLE-12) were exposed to hyperoxia to induce cell injury. Cell viability and apoptosis were detected, respectively, by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide) assay and flow cytometry. Inflammation and oxidative stress were evaluated by enzyme-linked immunosorbent serologic assay. Results: Hyperoxia decreased cell viability and promoted cell apoptosis of MLE-12. EDA2R was elevated in hyperoxia-induced MLE-12. Silencing of EDA2R enhanced cell viability and reduced cell apoptosis of hyperoxia-induced MLE-12. Hyperoxia-induced up-regulation of tumor necrosis factor alpha (TNF-α), Interleukin (IL)-1β, and IL-18 as well as MLE-12 was suppressed by knockdown of EDA2R. Inhibition of EDA2R down-regulated the level of malondialdehyde (MDA), up-regulated superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) in hyperoxia-induced MLE-12. Interference of EDA2R attenuated hyperoxia-induced increase in p-p65 in MLE-12. Conclusion: Knockdown of EDA2R exerted anti-inflammatory and antioxidant effects against hyperoxia-induced injury in lung epithelial cells through inhibition of nuclear factor kappa B (NF-κB) pathway.

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Section: Introductionmentioning

confidence: 99%

Knockdown of EDA2R alleviates hyperoxia-induced lung epithelial cell injury by inhibiting NF-κB pathway

Nan

Jia

Yang

et al. 2022

Allergol Immunopathol

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“…Based on the previous studies, 34 pancreatic tissues were excised, and fixed in 4% paraformaldehyde (catalog number: P1110, Solaibio), and embedded. The paraffin-embedded tissues were sectioned into 5-µm slices, and stained with HE (catalog number: G1120, Solaibio).…”

Section: Methodsmentioning

confidence: 99%

Administration of Akebia Saponin D Improved Blood Lipid Levels and Pregnancy Outcomes in Mice with Gestational Diabetes Mellitus

Chen,

Shi,

Zhang

2023

Balkan Med J

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Background: Gestational diabetes mellitus (GDM) is a prevalent and severe metabolic disease in pregnant women that is characterized by a high incidence. Placental oxidative stress and inflammation are recognized as the primary contributors to GDM pathogenesis. The repressive effect of akebia saponin D (ASD) on oxidative stress and inflammation has been demonstrated in various diseases. Aims: To investigate the impact of ASD on GDM. Study Design: Animal experimental study. Methods: GDM mice were intraperitoneally treated with ASD. The effect of ASD on GDM symptoms, blood lipid levels, pancreatic tissue damage, gestational outcomes, oxidative stress, and inflammation was assessed via intraperitoneal glucose and insulin tolerance tests, serum glucose and insulin level determination, lipid biochemistry analysis, pathological staining, oxidative stress evaluation, western blot analysis, and enzyme-linked immunosorbent assay. Results: ASD reduced the GDM-induced increase in body weight and blood glucose levels while restoring the decreased insulin levels associated with GDM. In addition, ASD improved the serum lipid parameters, pancreatic tissue damage, and gestational outcomes in GDM mice. Furthermore, ASD reversed the decreased levels of superoxide dismutase and glutathione while reducing the elevated concentrations of malondialdehyde and myeloperoxidase in GDM mice. In addition, ASD rescued the relative protein expression of nuclear factor-E2-related factor 2 and heme oxygenase-1 in the placenta of GDM mice. Additionally, ASD counteracted the increase in tumor necrosis factor-α, interleukin (IL)-6, and IL-1β levels in the sera and placenta of GDM mice. Conclusion: ASD suppressed oxidative stress and inflammation to effectively relieve symptoms and gestational outcomes of the GDM mice.

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“…Overexpression of clusterin, a glycoprotein expressed in airway epithelial cells, protected against hyperoxia-induced mitochondrial membrane disruption and prevented BCL2-associated X apoptosis regulator protein translocation, cytochrome C release, and caspase activation [ 363 ]. Inhibition of the ERK pathway by semaphorin 3A suppressed hyperoxia-induced apoptosis and inflammation [ 364 ]. Administration of chrysin (a flavonoid) attenuated lung damage via increased antioxidant activities (SOD and GSH), suppression of pro-inflammatory mediators (TNF-α and IL-1β), improving alveolarization, and reducing apoptosis (caspase 3) in an experimental model of hyperoxia-induced lung injury [ 365 ].…”

Section: Oxidative Stress and Inflammation In Hyperoxiamentioning

confidence: 99%

Oxidative Stress and Inflammation in Acute and Chronic Lung Injuries

Bezerra

Lanzetti

Nesi³

et al. 2023

Antioxidants

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Acute and chronic lung injuries are among the leading causes of mortality worldwide. Lung injury can affect several components of the respiratory system, including the airways, parenchyma, and pulmonary vasculature. Although acute and chronic lung injuries represent an enormous economic and clinical burden, currently available therapies primarily focus on alleviating disease symptoms rather than reversing and/or preventing lung pathology. Moreover, some supportive interventions, such as oxygen and mechanical ventilation, can lead to (further) deterioration of lung function and even the development of permanent injuries. Lastly, sepsis, which can originate extrapulmonary or in the respiratory system itself, contributes to many cases of lung-associated deaths. Considering these challenges, we aim to summarize molecular and cellular mechanisms, with a particular focus on airway inflammation and oxidative stress that lead to the characteristic pathophysiology of acute and chronic lung injuries. In addition, we will highlight the limitations of current therapeutic strategies and explore new antioxidant-based drug options that could potentially be effective in managing acute and chronic lung injuries.

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SEMA3A protects against hyperoxia-induced lung injury in a bronchopulmonary dysplasia model of newborn rat by inhibiting ERK pathway

Cited by 12 publications

References 32 publications

Knockdown of EDA2R alleviates hyperoxia-induced lung epithelial cell injury by inhibiting NF-κB pathway

Knockdown of EDA2R alleviates hyperoxia-induced lung epithelial cell injury by inhibiting NF-κB pathway

Administration of Akebia Saponin D Improved Blood Lipid Levels and Pregnancy Outcomes in Mice with Gestational Diabetes Mellitus

Oxidative Stress and Inflammation in Acute and Chronic Lung Injuries

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