The present study explored the protective effect of exogenous hydrogen sulfide (H2S) on lipopolysaccharide (LPS)‑induced acute kidney injury (AKI) and the underlying mechanisms. To establish an AKI injury mouse model, LPS (10 mg/kg) was intraperitoneally injected into mice pretreated with 0.8 mg/kg sodium hydrosulfide hydrate (NaHS), an H2S donor. The mouse survival rate and the degree of kidney injury were examined. To construct a cell damage model, HK‑2 cells were pretreated with different concentrations (0.1, 0.3 and 0.5 mM) of NaHS, and then the cells were stimulated with LPS (1 µg/ml). The cell viability, autophagy, apoptosis levels and the release of inflammatory factors were examined in mouse kidney tissue and HK‑2 renal tubular epithelial cells. It was found that pretreatment with NaHS significantly improved the survival rate of septic AKI mice, and reduced the renal damage, release of inflammatory factors and apoptosis. In HK‑2 cells, NaHS protected cells from LPS caused damage via promoting autophagy and inhibiting apoptosis and the release of inflammatory factors. In order to clarify the relationship between autophagy and apoptosis and inflammatory factors, this study used 3‑methyladenine (3‑MA) to inhibit autophagy. The results revealed that 3‑MA eliminated the protective effect of NaHS in HK‑2 cells and AKI mice. Overall, NaHS can protect from LPS‑induced AKI by promoting autophagy and inhibiting apoptosis and the release of inflammatory factors.
Keywords: acute kidney injury; apoptosis; autophagy; hydrogen sulfide; inflammation; lipopolysaccharides; sepsis.