کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8271623 | 1534981 | 2013 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cyclooxygenase-2 in newborn hyperoxic lung injury
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کلمات کلیدی
COX15-Hydroxy-prostaglandin dehydrogenaseTXASMCP-1HPGDSmPGESBALThromboxane A2 synthaseBPDcyclooxygenase - آنزیم سیکلواکسیژنازinterleukin - اینترلوکینthromboxane - ترومبوکسیانBronchopulmonary dysplasia - دیسپلازی ریویCyclooxygenase-2 - سیکلوکوکسیژناز2bronchoalveolar lavage - لارو برونکلو آلوئولارHyperoxia - هیپوکسیاmonocyte chemoattractant protein-1 - پروتئین شیمیایی monocyte chemoattractant-1Prostaglandins - پروستاگلاندین هاprostaglandin - پروستاگلاندینهاKeratinocyte-derived chemokine - کومکتین مشتق شده از کراتینوسیت
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Cyclooxygenase-2 in newborn hyperoxic lung injury Cyclooxygenase-2 in newborn hyperoxic lung injury](/preview/png/8271623.png)
چکیده انگلیسی
Supraphysiological O2 concentrations, mechanical ventilation, and inflammation significantly contribute to the development of bronchopulmonary dysplasia (BPD).Exposure of newborn mice to hyperoxia causes inflammation and impaired alveolarization similar to that seen in infants with BPD.Previously, we demonstrated that pulmonary cyclooxygenase-2 (COX-2) protein expression is increased in hyperoxia-exposed newborn mice.The present studies were designed to define the role of COX-2 in newborn hyperoxic lung injury.We tested the hypothesis that attenuation of COX-2 activity would reduce hyperoxia-induced inflammation and improve alveolarization.Newborn C3H/HeN micewere injected daily with vehicle, aspirin (nonselective COX-2 inhibitor), or celecoxib (selective COX-2 inhibitor) for the first 7 days of life.Additional studies utilized wild-type (C57Bl/6, COX-2+/+), heterozygous (COX-2+/-), and homozygous (COX-2-/-) transgenic mice.Micewere exposed to room air (21% O2) or hyperoxia (85% O2) for 14 days.Aspirin-injected and COX-2-/- pups had reduced levels of monocyte chemoattractant protein (MCP-1) in bronchoalveolar lavage fluid (BAL).Both aspirin and celecoxib treatment reduced macrophage numbers in the alveolar walls and air spaces.Aspirin and celecoxib treatment attenuated hyperoxia-induced COX activity, including altered levels of prostaglandin (PG)D2 metabolites.Decreased COX activity, however, did not prevent hyperoxia-induced lung developmental deficits.Our data suggest thatincreased COX-2 activity may contribute to proinflammatory responses, including macrophage chemotaxis, during exposure to hyperoxia.Modulation of COX-2 activity may be a useful therapeutic target to limit hyperoxia-induced inflammation in preterm infants at risk of developing BPD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 61, August 2013, Pages 502-511
Journal: Free Radical Biology and Medicine - Volume 61, August 2013, Pages 502-511
نویسندگان
Rodney D. Jr., Markus Velten, Trent E. Tipple, Leif D. Nelin, Lynette K. Rogers,