Melatonin protects against oxidative damage in a neonatal rat model of bronchopulmonary dysplasia

Pan, Li; Fu, Jianhua; Xue, Xindong; Xu, Wei; Zhou, Ping; Wei, Bing

doi:10.1007/s12519-009-0041-2

Cited by 36 publications

(31 citation statements)

References 25 publications

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“…Unfortunately, data on long-term respiratory outcomes of the studied cohorts were not provided. These clinical observations are in agreement with the demonstration in the mouse model of BPD that MT treatment reduces lung myeloperoxidase and nitrite/nitrate ratio and increases GPx, SOD and CAT activity (114). MT-treated animals showed significantly higher number of alveoli and less fibrotic aspects, suggesting that antioxidant effects of MT may positively influence alveolization and lung development under stressful conditions after preterm birth.…”

Section: Melatonin and Other Antioxidantssupporting

confidence: 90%

The Role of Genetic Polymorphisms in Antioxidant Enzymes and Potential Antioxidant Therapies in Neonatal Lung Disease

Dani

Poggi

2014

Antioxidants & Redox Signaling

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Significance: Oxidative stress is involved in the development of newborn lung diseases, such as bronchopulmonary dysplasia and persistent pulmonary hypertension of the newborn. The activity of antioxidant enzymes (AOEs), which is impaired as a result of prematurity and oxidative injury, may be further affected by specific genetic polymorphisms or an unfavorable combination of more of them. Recent Advances: Genetic polymorphisms of superoxide dismutase and catalase were recently demonstrated to be protective or risk factors for the main complications of prematurity. A lot of research focused on the potential of different antioxidant strategies in the prevention and treatment of lung diseases of the newborn, providing promising results in experimental models. Critical Issues: The effect of different genetic polymorphisms on protein synthesis and activity has been poorly detailed in the newborn, hindering to derive conclusive results from the observed associations with adverse outcomes. Therapeutic strategies that aimed at enhancing the activity of AOEs were poorly studied in clinical settings and partially failed to produce clinical benefits. Future Directions: The clarification of the effects of genetic polymorphisms on the proteomics of the newborn is mandatory, as well as the assessment of a larger number of polymorphisms with a possible correlation with adverse outcome. Moreover, antioxidant treatments should be carefully translated to clinical settings, after further details on optimal doses, administration techniques, and adverse effects are provided. Finally, the study of genetic polymorphisms could help select a specific high-risk population, who may particularly benefit from targeted antioxidant strategies.

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Section: Melatonin and Other Antioxidantssupporting

confidence: 90%

The Role of Genetic Polymorphisms in Antioxidant Enzymes and Potential Antioxidant Therapies in Neonatal Lung Disease

Dani

Poggi

2014

Antioxidants & Redox Signaling

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“…Similar to human infants who develop BPD (153), markers of oxidative stress are increased in hyperoxia-exposed mice (141) and rats (136). Together, these data suggest that hyperoxia may contribute to BPD and PH by several distinct mechanisms, including oxygen-mediated attenuation of HIF and VEGF signaling and oxygen-derived ROS.…”

Section: Hyperoxic Lung Injurymentioning

confidence: 82%

Role of Reactive Oxygen Species in Neonatal Pulmonary Vascular Disease

Wedgwood

Steinhorn

2014

Antioxidants & Redox Signaling

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Significance: Abnormal lung development in the perinatal period can result in severe neonatal complications, including persistent pulmonary hypertension (PH) of the newborn and bronchopulmonary dysplasia. Reactive oxygen species (ROS) play a substantive role in the development of PH associated with these diseases. ROS impair the normal pulmonary artery (PA) relaxation in response to vasodilators, and ROS are also implicated in pulmonary arterial remodeling, both of which can increase the severity of PH. Recent Advances: PA ROS levels are elevated when endogenous ROS-generating enzymes are activated and/or when endogenous ROS scavengers are inactivated. Animal models have provided valuable insights into ROS generators and scavengers that are dysregulated in different forms of neonatal PH, thus identifying potential therapeutic targets. Critical Issues: General antioxidant therapy has proved ineffective in reversing PH, suggesting that it is necessary to target specific signaling pathways for successful therapy. Future Directions: Development of novel selective pharmacologic inhibitors along with nonantioxidant therapies may improve the treatment outcomes of patients with PH, while further investigation of the underlying mechanisms may enable earlier detection of the disease.

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“…Previous studies have shown that pro-inflammatory cytokines were found to have increased in hyperoxia-exposed neonatal rodents and human neonates, [3][4][5] which indicates the important role of inflammatory responses in the pathogenesis of BPD. In addition, oxidative stress was also observed in hyperoxia treated neonatal rats, 6,7 and deletion of nuclear factor erythroid 2-related factor 2 (Nrf2) gene, an antioxidant gene, exacerbated hyperoxic lung injury in newborn mice. 8 The Wnt/b-catenin signalling pathway not only regulates cell fate and differentiation in the early stages of lung development, but also contributes to lung tissue structure maintenance.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol attenuates hyperoxia‐induced oxidative stress, inflammation and fibrosis and suppresses Wnt/β‐catenin signalling in lungs of neonatal rats

Zhao

Zhang

et al. 2015

Clin Exp Pharma Physio

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Although survival rate of infants born prematurely has been raised by supplemental oxygen treatment, it is followed by high morbidity of hyperoxia-induced bronchopulmonary dysplasia. In this study, the effect of resveratrol on the lung injury was evaluated in hyperoxia-exposed rats of preterm birth. The results demonstrated that hyperoxia led to thickened alveolar wall, simplified alveolar architecture and fibrosis. In addition, elevated methane dicarboxylic aldehyde level, decreased glutathione level and superoxide dismutase activity were also found in hyperoxic lungs, as well as the increased tumor necrosis factor-α, interleukin-1β and interleukin-6 in the bronchoalveolar lavage fluid. Fibrotic-associated proteins transforming growth factor-β1, α-smooth muscle actin, collagen I and fibronectin deposition were also found in interstitial substance of lungs. Furthermore, Wnt/β-catenin signalling was found to be active in hyperoxia-induced lungs. In addition, expression of SP-C was increased and T1α was decreased in hyperoxia-exposed lungs. Resveratrol intraperitoneal administration alleviated hyperoxia-induced histological injury of lungs, regulated redox balance, decreased pro-inflammatory cytokine release, and down-regulated expression of fibrotic-associated proteins. Furthermore, Wnt/β-catenin signalling was also suppressed by resveratrol, as represented by diminished expression of lymphoid enhancer factor-1, Wnt induced signalling protein-1 and cyclin D1. In addition, the increase of SP-C and decrease of T1α expression was prevented as well. The present study showed that resveratrol could protect lungs from hyperoxia-induced injury through its antioxidant, anti-inflammatory and anti-fibrotic effects. The transdifferentiation of alveolar epithelial type II cells to alveolar epithelial type I cells promotion and Wnt/β-catenin signalling suppression are also involved in the protective effect.

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Melatonin protects against oxidative damage in a neonatal rat model of bronchopulmonary dysplasia

Abstract: MT can reverse oxidants/antioxidants imbalance in damaged lung tissue and thus exert a beneficial effect on hyperoxia-induced lung disease in neonatal rats. With regard to humans, there may be a protective effect of MT on BPD.

Cited by 36 publications

References 25 publications

The Role of Genetic Polymorphisms in Antioxidant Enzymes and Potential Antioxidant Therapies in Neonatal Lung Disease

The Role of Genetic Polymorphisms in Antioxidant Enzymes and Potential Antioxidant Therapies in Neonatal Lung Disease

Role of Reactive Oxygen Species in Neonatal Pulmonary Vascular Disease

Resveratrol attenuates hyperoxia‐induced oxidative stress, inflammation and fibrosis and suppresses Wnt/β‐catenin signalling in lungs of neonatal rats

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