Suppression of NLRP3 inflammasome by Platycodin D via the TLR4/MyD88/NF-κB pathway contributes to attenuation of lipopolysaccharide induced acute lung injury in rats

•NLRP3 inflammasome is closely associated with the progression of Lung injury.•TLR4/MyD88/NF-kB pathway is important in the activation of NLRP3 inflammasome.•PLD can inhibit NLRP3 inflammasome activation.•Preventive administration of PLD attenuates LPS-induced lung injury. Acute lung injury (ALI) is a common clinical condition with a high mortality rate and no specific treatment is available. An excessive inflammatory response contributes to the development of ALI and accelerates its progression, and the NLRP3 inflammasome and NF-κB signaling pathways are key players in inflammation. Platycodin D has been reported to have anti-oxidant and anti-stress properties in various diseases. However, the effects of PLD in ALI has not been clearly demonstrated. The aim of this study was to investigate the therapeutic effects of PLD on ALI and its possible mechanism. Our study found that PLD pre-treatment attenuated lung histopathological injury in LPS-induced SD rats and reduced the levels of inflammatory cytokines and lung wet/dry ratio in bronchoalveolar lavage fluid (BALF). In addition, PLD modulate LPS-induced production of MDA, MPO, GSH, GSH-Px and CAT in lung tissue. In addition, PLD suppressed the activation of NLRP3 inflammatory microsomes and the NF-κB signaling pathway. Thus, our results suggest that PLD are protective against LPS-induced ALI by inhibiting NLRP3 and NF-κB signaling pathway.