Abstract
BackgroundAcute lung injury (ALI) is a serious disease with high incidence in ICU, and impaired mitochondria function plays a significant role in ALI. In this study, we examined the possible roles of exogenous hydrogen sulfide (H2S) in lung mitochondria regulation in ALI rats.MethodsThe rat ALI model was induced by an intra-tongue vein Lipopolysaccharide (LPS) injection. We used sodium hydrosulphide (NaHS) as the H2S donor. We randomly divided 40 Sprague–Dawley rats into five groups: control, LPS injury, LPS + low-dose NaHS (0.78 mg•kg-1), LPS + middle-dose NaHS (1.56 mg•kg-1), and LPS + high-dose NaHS (3.12 mg•kg-1). Rats were killed 3 h after NaHS administration. We calculated a semi-quantitative histological index of lung injury assessments and measured the lung wet-to-dry weight ratio. We further analyzed serum for interleukin-1β levels using enzyme-linked immunosorbent assays. We observed lung mitochondria ultrastructures with an electron microscope. We examined oxidative stress markers in lung mitochondria and the mitochondrial swelling and activity. We analyzed lung mitochondria and cytosol Cyt-c protein expression using Western blotting.ResultsCompared to the control group, the quantitative assessment score index, wet-to-dry weight ratios, and interleukin-1β content in the LPS injury group were significantly increased and the mitochondrial ultrastructure damaged. Furthermore, mitochondrial activity, adenosine triphosphatease, superoxide dismutase, glutathione peroxidase, and mitochondrial Cyt-c protein expression were significantly decreased, and malondialdehyde content, mitochondrial swelling, and cytosol Cyt-c protein expression were significantly increased in the LPS injury group compared to the control group. These effects were lessened by NaHS.ConclusionExogenous H2S provided a protective effect against ALI by decreasing the mitochondrial lipid peroxidation level and protecting the cell structure in the LPS-induced rat models. Its regulatory effect on lung mitochondria is positively correlated with the dosage.
Highlights
Acute lung injury (ALI) is a serious disease with high incidence in ICU, and impaired mitochondria function plays a significant role in ALI
Histological lung tissue changes in each group We found that the control group morphology was normal with light microscopy, and there was no alveolar edema fluid in the alveolar space
The LPS injury group showed diffuse edema in alveolar spaces, lung interstitium, hemorrhage, severe inflammatory cell infiltration, serous exudation in the alveolar space, and a thickened interbular septa like “hyaline membrane”. These changes were lightly mitigated in the LPS + low-dose Sodium hydrosulfide (NaHS) group, and significantly mitigated in LPS + middle-dose and high-dose NaHS groups (Figure 1)
Summary
Acute lung injury (ALI) is a serious disease with high incidence in ICU, and impaired mitochondria function plays a significant role in ALI. Sepsis (the presence of pus-forming bacteria or their toxins in the blood or tissues) is one of the most important ALI/ARDS causes [3]. Lipopolysaccharide (LPS), a major gram-negative bacillary endotoxin component, plays an important role in initiating inflammatory response and causing systemic inflammatory response syndrome (SIRS) and sepsis. ALI induced by LPS is an acute pulmonary inflammation response in the lung, in which the accumulation and activation of polymophonuclear neutrophil (PMN) and oxygen free radical release are the key links [4]. Inflammatory cell activation and increased oxidative stress are implicated in this pathogenesis [6]. Malondialdehyde [MDA], an end-product of membrane lipid peroxidation, adenosine triphosphatease [ATPase], anti-oxidants superoxide dismutase [SOD], and glutathione peroxidase [GPx] are currently considered the basic oxidative stress markers
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