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首页> 外文期刊>Journal of Cellular Physiology >Autophagy maintains the integrity of endothelial barrier in LPS‐induced lung injury
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Autophagy maintains the integrity of endothelial barrier in LPS‐induced lung injury

机译:自噬维持内皮的完整性障碍在LPS诱导肺损伤

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Understanding the role and underlying regulation mechanism of autophagy in lipopolysaccharide‐induced lung injury (LPS‐LI) may provide potentially new pharmacological targets for treatment of acute lung injury. The aim of this study was to investigate the functional significance of autophagy in LPS‐LI. The autophagy of human pulmonary microvascular endothelial cells (HPMVECs) and mice was inhibited before they were challenged with LPS. In vitro, permeability, vitality, and the LDH release rate of the cells were detected, the zonula occluden‐1 (ZO‐1) expression and the stress fiber formation were determined. In vivo, the lung injury was assessed. We found LPS caused high permeability and increased lactate dehydrogenase (LDH) release rate, lowered viability of the cells, inhibited the ZO‐1 expression and induced stress fiber formation, these effects were further aggravated by prohibiting the level of autophagy. Consistently, in in vivo experiments, LPS‐induced serious lung injury, which was reflected as edema, leukocyte infiltration and hemorrhage in lung tissue, and the high concentration of pro‐inflammation cytokines tumor necrosis factor (TNF)‐α and interleukin (IL)‐1β in bronchoalveolar lavage fluid (BALF). Inhibiting autophagy further exacerbated LPS‐LI. It appears that autophagy played a protective role in LPS‐LI in part through restricting the injury of lung microvascular barrier.
机译:理解和潜在的调控作用自噬的机制脂多糖所致诱导肺损伤(李LPS所致)可以提供潜在的新的药理吗目标治疗急性肺损伤。本研究的目的是调查自噬的功能意义在LPS所致。自噬的人类肺微血管内皮细胞(HPMVECs)和老鼠抑制前与有限合伙人的挑战。体外、渗透率、活力和LDH释放率的细胞被检测到,zonula occluden 1(佐薇还是1)表达式和应力纤维形成测定。肺损伤评估。高磁导率和乳酸增加脱氢酶(LDH)释放率,降低了生存能力的细胞,抑制了佐薇量1表达和诱导应力纤维的形成,这些影响是进一步加重禁止自噬的水平。在体内实验中,LPS诱导严重肺部伤,反映为水肿、白细胞在肺组织渗透和出血,高浓度的pro的炎症细胞因子肿瘤坏死因子(TNF)的α和白细胞介素(IL)‐1β在bronchoalveolar灌洗流体(BALF)。加剧了LPS所致。发挥了保护作用有限合伙人应承担的部分通过限制肺的损伤微血管屏障。

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