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首页> 外文期刊>Medical Gas Research >Inhaled hydrogen sulfide protects against lipopolysaccharide-induced acute lung injury in mice
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Inhaled hydrogen sulfide protects against lipopolysaccharide-induced acute lung injury in mice

机译：吸入硫化氢可预防脂多糖诱导的小鼠急性肺损伤

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Background Local pulmonary and systemic infections can lead to acute lung injury (ALI). The resulting lung damage can evoke lung failure and multiple organ dysfunction associated with increased mortality. Hydrogen sulfide (H2S) appears to represent a new therapeutic approach to ALI. The gas has been shown to mediate potent anti-inflammatory and organ protective effects in vivo. This study was designed to define its potentially protective role in sepsis-induced lung injury. Methods C57BL/6 N mice received lipopolysaccharide (LPS) intranasally in the absence or presence of 80 parts per million H2S. After 6 h, acute lung injury was determined by comparative histology. Bronchoalveolar lavage (BAL) fluid was analyzed for total protein content and differential cell counting. BAL and serum were further analyzed for interleukin-1β, macrophage inflammatory protein-2, and/or myeloperoxidase glycoprotein levels by enzyme-linked immunosorbent assays. Differences between groups were analyzed by one way analysis of variance. Results Histological analysis revealed that LPS instillation led to increased alveolar wall thickening, cellular infiltration, and to an elevated ALI score. In the presence of H2S these changes were not observed despite LPS treatment. Moreover, neutrophil influx, and pro-inflammatory cytokine release were enhanced in BAL fluid of LPS-treated mice, but comparable to control levels in H2S treated mice. In addition, myeloperoxidase levels were increased in serum after LPS challenge and this was prevented by H2S inhalation. Conclusion Inhalation of hydrogen sulfide protects against LPS-induced acute lung injury by attenuating pro-inflammatory responses.
机译：背景技术局部肺部和全身感染可导致急性肺损伤（ALI）。导致的肺部损伤可引起肺衰竭和多器官功能障碍，并伴有死亡率增加。硫化氢（H 2 S）似乎代表了一种新的ALI治疗方法。该气体已显示出在体内介导有效的抗炎和器官保护作用。本研究旨在确定其在败血症诱导的肺损伤中的潜在保护作用。方法C57BL / 6 N小鼠在不存在或存在80 ppm的H 2 S的情况下经鼻腔接受脂多糖（LPS）。 6小时后，通过比较组织学确定急性肺损伤。分析支气管肺泡灌洗液（BAL）的总蛋白含量和差异细胞计数。通过酶联免疫吸附试验进一步分析BAL和血清中白介素-1β，巨噬细胞炎性蛋白2和/或髓过氧化物酶糖蛋白水平。组之间的差异通过一种方差分析来分析。结果组织学分析显示，LPS滴注导致肺泡壁增厚，细胞浸润和ALI评分升高。尽管进行了LPS处理，但在H 2 S存在下仍未观察到这些变化。此外，LPS处理的小鼠的BAL液中嗜中性粒细胞的流入和促炎性细胞因子的释放增加，但与H 2 S处理的小鼠的对照水平相当。此外，LPS激发后血清中过氧化物酶水平升高，这可以通过吸入H 2 S来预防。结论吸入硫化氢可减轻LPS引起的急性肺损伤，从而减轻炎症反应。

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