Propylene glycol alginate sodium sulphate attenuates LPS-induced acute lung injury in a mouse model.

Propylene glycol alginate sodium sulphate, a sulphated polysaccharide, has been used to treat hyperlipidaemia and ischaemia–reperfusion injury of liver. This study aimed to investigate the effect of propylene glycol alginate sodium sulphate on LPS-induced acute lung injury. Propylene glycol alginate sodium sulphate was injected intraperitoneally into male C57BL/6 mice with or without LPS administration. Survival rates were calculated. Serum, bronchoalveolar lavage fluid and lung tissues were collected to determine lung histology, wet/dry ratio, Evans blue albumin permeability, protein levels, the counts of immune cells and the levels of inflammatory cytokines and chemokines. Serum alanine aminotransferase, aspartate transaminase, creatinine and blood urea nitrogen levels were also measured. Additionally, NF-κB signalling was detected in the lung. Propylene glycol alginate sodium sulphate treatment significantly improved the survival of mice suffering from LPS. Lung histological injury, wet/dry ratio, Evans blue albumin permeability, neutrophils and the inflammatory cytokines and chemokines were significantly reduced by propylene glycol alginate sodium sulphate treatment. NF-κB signalling was significantly inhibited by propylene glycol alginate sodium sulphate in the lung of mice subjected to LPS. Furthermore, serum alanine aminotransferase, aspartate transaminase, creatinine and blood urea nitrogen levels were also significantly decreased after propylene glycol alginate sodium sulphate administration. This study suggests that NF-κB signalling and inhibition of pro-inflammatory cytokines, chemokines and neutrophil accumulation may be involved in the process of acute lung injury attenuation by propylene glycol alginate sodium sulphate.