Protective effects of exogenous hydrogen sulfide on seawater aspiration induced-acute lung injury in rats

Aim: Seawater drowning induced-acute lung injury (ALI) is a serious clinical condition characterized by refractory hypoxemia, enhanced alveolar-capillary permeability, hemorrhage, and uncontrolled overwhelming inflammatory responses. Hydrogen sulfide (H2S) is an endogenous gaseous mediator that plays an important role in the physiological and pathophysiological conditions, especially in some inflammatory diseases. However, the beneficial effects of sodium hydrosulfide (NaHS), a H2S donor, on seawater aspiration-induced ALI remains to be elucidated. Material and methods: Two hundred and forty rats were equally assigned to the naive group, normal saline group, seawater group, or seawater + NaHS group. NaHS or vehicle was intraperitoneally administered immediately after seawater aspiration. Arterial blood gas analysis was performed with a gas analyzer at baseline, 30 min, 1 h, 4 h, and 24 h after the seawater aspiration, respectively. Histological scores, computed tomography scan, TUNE-positive cells assay, Toll-like receptor 4, nuclear factor kappa B p65, caspase-3, tumor necrosis factor-alpha, interleukin (IL)-1β, IL-6, IL-10, wet-to-dry weight ratio, myeloperoxidase activity, malondialdehyde, and superoxide dismutase levels in the lung were assessed at 30 min after the seawater aspiration. Results: NaHS treatment alleviated ALI as demonstrated by the increased arterial partial oxygen tension and deceased lung histological scores, which was accompanied by decreased TUNEL-positive cells, Toll-like receptor 4, nuclear factor kappa B p65, caspase-3, tumor necrosis factor-alpha, IL-1β, myeloperoxidase activity, and malondialdehyde in the lung. Conclusions: Our study suggested that the protective effects of NaHS on seawater aspiration-induced ALI might be associated with its antiinflammatory, anti-oxidative, and anti-apoptotic properties.