Echinacoside attenuates lipopolysaccharide-induced acute lung injury in newborn mice via inactivation of NF-κB/NLRP3 signaling pathway

Purpose: To investigate the effect of echinacoside (ECH) on acute lung injury (ALI) and the underlying mechanism of action. Methods: The ALI model was established through intranasal instillation of lipopolysaccharide (LPS). Lung tissue damage was determined using hematoxylin and eosin (H&E) staining and lung wet-to-dry-weight ratio. Bronchoalveolar lavage fluid (BALF) protein concentration, cell count, and cytokine level were evaluated. Western blotting was used to determine protein expression level. Results: ECH attenuated lung tissue injury and lung wet-to-dry-weight ratio in the ALI model (p < 0.01). The total protein content and number of total cells, neutrophils, and macrophages increased in BALF of mice treated with LPS, but these increases were reversed by ECH treatment (p < 0.01). The levels of TNF-alpha and IL-1 beta increased in BALF and lung tissue of LPS-treated mice; however, ECH treatment decreased these changes (p < 0.01). In addition, ECH inhibited the activation of the nuclear factor-kappa B (NF-kappa B)/NLR family pyrin domain containing 3 (NLRP3) pathway in LPS-treated mice (p < 0.01). Conclusion: Echinacoside attenuates LPS-induced ALI via inactivation of the NF-kappa B/NLRP3 pathway, making echinacoside a potential drug for the treatment of ALI.