Autophagy Plays a Protective Role in Sodium Hydrosulfide-Induced Acute Lung Injury by Attenuating Oxidative Stress and Inflammation in Rats.

ABSTRACT

Sodium hydrosulfide (NaHS), as an exogenous hydrogen sulfide (H2S) donor, has been used in various pathological models. NaHS is usually considered to be primarily protective, however, the toxic effect of NaHS has not been well elucidated. The aim of this study was to investigate whether NaHS (1 mg/kg) can induce acute lung injury (ALI is a disease process characterized by diffuse inflammation of the lung parenchyma) and define the mechanism by which NaHS-induced ALI involves autophagy, oxidative stress, and inflammatory response. Wistar rats were randomly divided into three groups (control group, NaHS group, and 3-MA + NaHS group), and samples from each group were collected from 2, 6, 12, and 24 h. We found that intraperitoneal injection of NaHS (1 mg/kg) increased the pulmonary levels of H2S and oxidative stress-related indicators (reactive oxygen species, myeloperoxidase, and malondialdehyde) in a time-dependent manner. Intraperitoneal injection of NaHS (1 mg/kg) induced histopathological changes of ALI and inhibition of autophagy exacerbated the lung injury. This study demonstrates that administration of NaHS (1 mg/kg) induces ALI in rats and autophagy in response to ROS is protective in NaHS-induced ALI by attenuating oxidative stress and inflammation.