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首页> 外文期刊>BMC Pulmonary Medicine >Caffeine is associated with improved alveolarization and angiogenesis in male mice following hyperoxia induced lung injury
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Caffeine is associated with improved alveolarization and angiogenesis in male mice following hyperoxia induced lung injury

机译：咖啡因与高氧诱导的肺损伤后雄性小鼠肺泡化和血管生成改善有关

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Caffeine therapy for apnea of prematurity reduces the incidence of bronchopulmonary dysplasia (BPD) in premature neonates. Several mechanisms, including improvement in pulmonary mechanics underly beneficial effects of caffeine in BPD. As vascular development promotes alveologenesis, we hypothesized that caffeine might enhance angiogenesis in the lung, promoting lung growth, thereby attenuating BPD. C57Bl/6 mice litters were randomized within 12?h of birth to room air (RA) or 95%O2 to receive caffeine (20?mg/kg/day) or placebo for 4 days and recovered in RA for 12wks. The lung mRNA and protein expression for hypoxia-inducible factors (HIF) and angiogenic genes performed on day 5. Lung morphometry and vascular remodeling assessed on inflation fixed lungs at 12wks. Caffeine and hyperoxia in itself upregulate HIF-2α and vascular endothelial growth factor gene expression. Protein expression of HIF-2α and VEGFR1 were higher in hyperoxia/caffeine and angiopoietin-1 lower in hyperoxia. An increase in radial alveolar count, secondary septal count, and septal length with a decrease in mean linear intercept indicate an amelioration of hyperoxic lung injury by caffeine. An increase in vessel surface area and a significant reduction in smooth muscle thickness of the pulmonary arterioles may suggest a beneficial effect of caffeine on vascular remodeling in hyperoxia, especially in male mice. Postnatal caffeine by modulating angiogenic gene expression early in lung development may restore the pulmonary microvasculature and alveolarization in adult lung.
机译：咖啡因治疗早产儿呼吸暂停可降低早产儿支气管肺发育不良（BPD）的发生率。几种机制，包括改善肺力学，对咖啡因在BPD中的有益作用均不足。随着血管的发展促进肺泡生成，我们假设咖啡因可能会增强肺部的血管生成，从而促进肺部生长，从而减弱BPD。 C57Bl / 6小鼠产仔在出生后12小时内随机分配到室内空气（RA）或95％O2中，以接受咖啡因（20？mg / kg /天）或安慰剂治疗4天，并在RA中恢复12周。在第5天进行缺氧诱导因子（HIF）和血管生成基因的肺mRNA和蛋白表达。在12周时对充气固定的肺评估肺形态和血管重塑。咖啡因和高氧本身会上调HIF-2α和血管内皮生长因子基因的表达。 HIF-2α和VEGFR1的蛋白表达在高氧/咖啡因中较高，而血管生成素-1在高氧中较低。放射状肺泡计数，继发间隔数和间隔长度的增加以及平均线性截距的减少表明咖啡因可减轻高氧性肺损伤。血管表面积的增加和肺小动脉平滑肌厚度的显着减少可能表明咖啡因对高氧症，特别是雄性小鼠的血管重塑具有有益作用。产后咖啡因可通过调节肺发育早期的血管生成基因表达而恢复成年肺的肺微血管和肺泡形成。

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