Abstract: Objective: To study the structure of BRAP-1, an acidic polysaccharide from Brassica rapa L. and its effect and mechanism on lipopolysaccharide (LPS)-induced lung injury in mice. Methods: The chemical composition, molecular mass, structure and monosaccharide composition were analyzed by the phenol-sulfuric acid method, the m-hydroxydiphenyl method, the Coomassie brilliant blue method, high performance gel permeation chromatography (HPGPC), Fourier transform infrared (FT-IR) spectroscopy and gas chromatography-mass chromatography (GC-MS). The mice in the control and model groups were gavaged with 0.5 mL/d of phosphate buffered saline (PBS) and those in the BRAP-1 groups 50, 100 and 200 mg/(kg mb·d) of BRAP-1 for 10 days, respectively. A lung injury model was established by intratracheal LPS infusion. Lung wet/dry mass ratio, broncho-alveolar lavage fluid (BALF) protein concentration and total cell count were measured and hematoxylin-eosin (HE) staining was performed to evaluate histopathological changes. An enzyme-linked immunosorbent assay (ELISA) was used to determine the contents of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-10 and interferon-γ (IFN-γ) in the serum of mice in each group. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the mRNA expression of tumor necrosis factor receptor (TNFR), Toll-like receptor 4 (TLR4), nuclear factor kappa B p65 (NF-κB p65), IL-1β and NOD-like receptor 3 (NLRP3) in lung tissue. Results: Compared with the model group, BRAP-1 alleviated the pathological changes of lung tissue such as edema, alveolar infiltration, protein exudation and excessive cytokines release in mice with lung injury, and significantly decreased the mRNA expression of key genes in the NF-κB/NLRP3 signaling pathway. Conclusion: BRAP-1 has a significantly protective effect on LPS-induced lung injury in mice, and the mechanism may be associated with the regulation of the NF-κB/NLRP3 signaling pathway.

Key words: Brassica rapa L. acidic polysaccharide; lung injury; protective effect; NF-κB/NLRP3 pathway