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Hexarelin modulates lung mechanics, inflammation, and fibrosis in acute lung injury

机译：Hexarelin在急性肺损伤中调节肺部力学，炎症和纤维化

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ABSTRACT Introduction: Acute respiratory distress syndrome (ARDS) is an acute form of diffuse lung injury characterized by (i) an intense inflammatory response, (ii) increased pulmonary vascular permeability, and (iii) the loss of respiratory pulmonary tissue. In this article we explore the therapeutic potential of hexarelin, a synthetic hexapeptide growth hormone secretagogue (GHS), in an experimental model of ARDS. Hexarelin has anti-inflammatory properties and demonstrates cardiovascular-protective activities including the inhibition of cardiomyocyte apoptosis and cardiac fibrosis, both of which may involve the angiotensin-converting enzyme (ACE) system. Methods: In our experimental model, ARDS was induced by the instillation of 100 mM HCl into the right bronchus; these mice were treated with hexarelin (320 μg/kg, ip) before (Pre) or after (Post) HCl challenge, or with vehicle. Respiratory system compliance, blood gas analysis, and differential cell counts in a selective bronchoalveolar lavage (BAL) were determined 6 or 24 hours after HCl instillation. In an extended study, mice were observed for a subsequent 14 days in order to assess lung fibrosis. Results: Hexarelin induced a significant improvement in lung compliance and a reduction of the number of total immune cells in BAL 24 hours after HCl instillation, accompanied with a lower recruitment of neutrophils compared with the vehicle group. At day 14, hexarelin-treated mice presented with less pulmonary collagen deposition compared with vehicle-treated controls. Conclusions: Our data suggest that hexarelin can inhibit the early phase of the inflammatory response in a murine model of HCl-induced ARDS, thereby blunting lung remodeling processes and fibrotic development.
机译：摘要介绍：急性呼吸窘迫综合征（ARDS）是一种急性形式的弥漫性肺损伤，其特征在于（i）强烈的炎症反应，（ii）增加肺血管渗透性和（iii）呼吸肺组织的丧失。在本文中，我们在ARDS的实验模型中探讨了六种六肽生长激素促分泌素（GHS）的六六肽的治疗潜力。 Hexarelin具有抗炎性质，并证明了心血管保护活性，包括抑制心肌细胞凋亡和心肌纤维化，这两种可能涉及血管紧张素转换酶（ACE）系统。方法：在我们的实验模型中，通过将100mm HCl滴注到右支气管的滴注诱导ARDS;将这些小鼠用六碱（320μg/ kg，IP）处理（pre）或后（发布）HCl攻击或用载体处理。在HCl灌注后6或24小时测定选择性支气管肺泡灌洗（BAL）中的呼吸系统依从性，血液气体分析和差异细胞计数。在一项延长的研究中，观察到后续14天的小鼠以评估肺纤维化。结果：Hexarelin诱导肺顺应性的显着改善，并在HCl滴注后24小时内减少了HL 24小时的总免疫细胞数量，与载体组相比，较低招募中性粒细胞。与载体处理的对照相比，在第14天，用较低的肺胶原沉积提出了六种肺胶原沉积的小鼠。结论：我们的数据表明，Hexarelin可以抑制HCl诱导的ARDS小鼠模型中炎症反应的早期阶段，从而延长肺重塑过程和纤维化发育。

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