Esechie Aimalohi, Kiss Levente, Olah Gabor, Horváth Eszter M, Hawkins Hal, Szabo Csaba, Traber Daniel L
Department of Neuroscience and Cell Biology, The University of Texas Medical Branch, Galveston, TX 77555, USA.
Clin Sci (Lond). 2008 Aug;115(3):91-7. doi: 10.1042/CS20080021.
Acute lung injury results in a severe inflammatory response, which leads to priming and activation of leucocytes, release of reactive oxygen and reactive nitrogen species, destruction of pulmonary endothelium, extravasation of protein-rich fluid into the interstitium and formation of oedema. Recently, H2S (hydrogen sulfide) has been shown to decrease the synthesis of pro-inflammatory cytokines, reduce leucocyte adherence to the endothelium and subsequent diapedesis of these cells from the microvasculature in in vivo studies, and to protect cells in culture from oxidative injury. In the present study, we hypothesized that a parenteral formulation of H2S would reduce the lung injury induced by burn and smoke inhalation in a novel murine model. H(2)S post-treatment significantly decreased mortality and increased median survival in mice. H2S also inhibited IL (interleukin)-1beta levels and significantly increased the concentration of the anti-inflammatory cytokine IL-10 in lung tissue. Additionally, H2S administration attenuated protein oxidation following injury and improved the histological condition of the lung. In conclusion, these results suggest that H2S exerts protective effects in acute lung injury, at least in part through the activation of anti-inflammatory and antioxidant pathways.
急性肺损伤会引发严重的炎症反应，导致白细胞的启动和激活、活性氧和活性氮物质的释放、肺内皮的破坏、富含蛋白质的液体渗入间质以及水肿的形成。最近，在体内研究中发现，硫化氢（H2S）可减少促炎细胞因子的合成，降低白细胞与内皮的黏附以及随后这些细胞从微血管的渗出，并保护培养中的细胞免受氧化损伤。在本研究中，我们假设一种肠胃外给药的H2S制剂会在一种新型小鼠模型中减轻烧伤和烟雾吸入诱导的肺损伤。H2S治疗后显著降低了小鼠的死亡率并提高了中位生存期。H2S还抑制了肺组织中白细胞介素（IL）-1β水平，并显著提高了抗炎细胞因子IL-10的浓度。此外，给予H2S减轻了损伤后的蛋白质氧化，并改善了肺的组织学状况。总之，这些结果表明H2S在急性肺损伤中发挥保护作用，至少部分是通过激活抗炎和抗氧化途径实现的。
