Hydrogen-rich saline regulates the polarization and apoptosis of alveolar macrophages and attenuates lung injury via suppression of autophagy in septic rats

Peng Qiu; Yang Liu; Keyan Chen; Youjing Dong; Shiqing Liu; Jin Zhang

doi:10.21037/atm-21-2489

Hydrogen-rich saline regulates the polarization and apoptosis of alveolar macrophages and attenuates lung injury via suppression of autophagy in septic rats

Ann Transl Med. 2021 Jun;9(12):974. doi: 10.21037/atm-21-2489.

Authors

Peng Qiu¹, Yang Liu², Keyan Chen³, Youjing Dong¹, Shiqing Liu¹, Jin Zhang¹

Affiliations

¹ Department of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, China.
² Department of Oncology, Shengjing Hospital of China Medical University, Shenyang, China.
³ Department of Laboratory Animal Science, China Medical University, Shenyang, China.

Abstract

Background: Hydrogen-rich saline (HRS) has a protective effect on sepsis-induced lung injury. However, the underlying mechanisms are still unclear. Polarization and apoptosis of macrophages are essential factors in the pathogenesis of acute lung injury (ALI). Moreover, autophagy is involved in the regulation of both macrophage polarization and apoptosis. Therefore, this study investigated the ability of HRS to attenuate ALI through regulation of the polarization and apoptosis of alveolar macrophages (AMs) during sepsis by modulating autophagy.

Methods: Male Sprague-Dawley (SD) rats were used to prepare the sepsis-induced lung injury animal model. Rat lung tissue was harvested after lipopolysaccharide (LPS) treatment, in the presence or absence of HRS, and the AMs were analyzed for changes in polarization, apoptosis, and autophagy. The rat AM cell line NR8383 was used to examine these processes in vitro using Western blot analysis, flow cytometry, and transmission electron microscopy.

Results: LPS-induced ALI in rats was associated with an increase in autophagy, apoptosis, and M1 polarization but a decrease in M2 polarization in AMs. These effects were reversed by administration of HRS. Inhibition of AM autophagy with 3-methyladenine (3-MA) decreased apoptosis and M1 polarization and increased M2 polarization, paralleling the effects of HRS.

Conclusions: HRS could attenuate ALI in septic rats through regulation of AM polarization and a reduction in apoptosis by suppressing autophagy. This may represent a potential novel therapeutic target for the treatment of ALI caused by sepsis.

Keywords: Hydrogen-rich saline (HRS); acute lung injury (ALI); apoptosis; autophagy; macrophage; polarization.