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首页> 外文期刊>American Journal of Physiology >Interleukin~(-1)0 protects cultured fetal rat type II epithelial cells from injury induced by mechanical stretch
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Interleukin~(-1)0 protects cultured fetal rat type II epithelial cells from injury induced by mechanical stretch

机译：白细胞介素〜（-1）0保护培养的胎儿大鼠II型上皮细胞免受机械拉伸诱导的损伤

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First published December 7, 2007; doi:10.1152/ajplung.00370.2007.-Mechanical ventilation plays a central role in the pathogenesis of bronchopulmonary dysplasia. However, the mechanisms by which excessive stretch of fetal or neonatal type II epithelial cells contributes to lung injury are not well defined. In these investigations, isolated embryonic day 19 fetal rat type II epithelial cells were cultured on substrates coated with fibronectin and exposed to 5% or 20% cyclic stretch to simulate mechanical forces during lung development or lung injury, respectively. Twenty percent stretch of fetal type II epithelial cells increased necrosis, apoptosis, and proliferation compared with control, unstretched samples. By ELISA and real-time PCR (qRT-PCR), 20% stretch increased secretion of IL-8 into the media and IL-8 gene expression and inhibited IL~(-1)0 release. Interestingly, administration of recombinant IL~(-1)0 before 20% stretch did not affect cell lysis but significantly reduced apoptosis and IL-8 release compared with stretched samples without IL~(-1)0. Collectively, our studies suggest that IL~(-1)0 may play an important role in protection of fetal type fl epithelial cells from injury secondary to stretch.
机译：2007年12月7日第一次出版; DOI：10.1152 / AJPLUNG.00370.2007。 - 机械通风在支气管扩漏性发育不良的发病机制中起着重要作用。然而，过度胎儿或新生儿II型上皮细胞有助于肺损伤的机制并不明确。在这些研究中，孤立的胚胎第19天19胎儿大鼠II型上皮细胞在涂有纤连蛋白涂覆的底物上培养，并暴露于5％或20％的循环拉伸，以模拟肺部发育或肺损伤期间的机械力。 20％的胎儿II型上皮细胞的胎儿上皮细胞增加坏死，细胞凋亡和增殖与对照，未避免的样品相比。通过ELISA和实时PCR（QRT-PCR），20％拉伸将IL-8分泌进入培养基和IL-8基因表达并抑制IL〜（-1）0释放。有趣的是，在20％拉伸之前的重组IL〜（-1）0的给药不影响细胞裂解，但与没有IL〜（-1）0的拉伸样品相比，细胞凋亡和IL-8释放。统称，我们的研究表明IL〜（-1）0可能在保护胎儿型FL上皮细胞免受继发性的伤害中发挥重要作用。

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