Bupleurum chinense DC.–Derived Acidic Polysaccharide: Alleviates Lipopolysaccharide-Induced Acute Lung Injury via Activation of Siglec-E

Background: Acute lung injury (ALI) is linked to neutrophil extracellular traps (NETs). BP polysaccharides from Bupleurum chinense DC. modulate neutrophil function, but their effects on NET formation, release, or degradation are unknown. Purpose: This study tested whether BP-1, an acidic polysaccharide from Bupleurum chinense DC., attenuates NET formation in murine ALI by activating Siglec-E. Methods: BP-1, an acidic polysaccharide isolated from Bupleurum chinense DC. and confirmed to bind human Siglec-9 and murine Siglec-E, was physicochemically characterized by SEM, FT-IR, and HPLC. A murine ALI model was induced by intratracheal LPS administration, and the anti-inflammatory effects and molecular mechanisms of BP-1 were systematically evaluated using H&E staining, BALF cytokine analysis, Western blotting, immunofluorescence, and immunohistochemistry. To determine murine Siglec-E dependency, primary neutrophils were isolated from Siglec-EPKO mice and stimulated with nigericin in vitro; NET formation was assessed by immunofluorescence staining. Results: BP-1 contains 81.62% carbohydrates, mainly GalA, Glc, Gal, and Ara. In murine LPS-induced ALI, BP-1 reduced neutrophil infiltration and NET formation—evidenced by lower MPO activity, Cit-H3, and dsDNA in lung tissue and BALF. It also decreased serum IL-1β and TNF-α, and suppressed pulmonary PAD4. In primary neutrophils, BP-1 inhibited nigericin-induced NETs only in the presence of murine Siglec-E; no effect was seen in Siglec-EPKO cells. BLI confirmed that BP-1 binds murine Siglec-E. Conclusion: BP-1 binds Siglec-E and inhibits neutrophil recruitment and NET formation in a mouse model of ALI.