Saturated hydrogen saline attenuates endotoxin-induced lung dysfunction

Background: Acute lung injury induced by lipopolysaccharides (LPSs) is caused by pulmonary inflammation and pulmonary vascular permeability. Activation of p38 mitogen-activated protein kinase causes inflammation, and proinflammatory cytokines and oxidative stress induce autophagy, a catabolic mechanism responsible for protein degradation and recycling of damaged proteins and cytoplasmic organelles. If not controlled, excessive autophagy responses can result in cell death. Materials and methods: In this study, we pretreated rats with saturated hydrogen saline, and examined the molecular mechanism by which saturated hydrogen saline attenuates LPS-induced acute lung dysfunction. Sixty-four male Sprague-Dawley rats were randomly assigned to one of three groups-a control group, an LPS group, or an LPS plus saturated hydrogen saline (LPS + H-2) group. Results: Treatment with saturated hydrogen saline prolonged the median survival time of rats and reduced lung dysfunction induced by LPS. Moreover, saturated hydrogen saline significantly attenuated LPS-mediated induction of serum tumor necrosis factor a, interleukin 6, myeloperoxidase, and malondialdehyde (P < 0.05). Conclusions: Autophagosomes were found in the cytoplasm of type II alveolar epithelial cells of LPS-treated rats, and light chain 3 protein (LC3)I/ II was increased by LPS treatment. In contrast, saturated hydrogen saline decreased the number of autophagosomes and LC3I/II expression. Saturated hydrogen saline also attenuated the LPS-mediated increase in apoptosis and p38 expression. Taken together, saturated hydrogen saline may attenuate LPS-induced acute lung dysfunction in rats by reducing inflammation, autophagy, and apoptosis involving the p38 mitogen-activated protein kinase signaling pathway. (C) 2015 Elsevier Inc. All rights reserved.