Bupleurum chinense DC.–Derived Acidic Polysaccharide: Alleviates Lipopolysaccharide-Induced Acute Lung Injury via Activation of Siglec-E
- 1Department of Pharmaceutics, Faculty of Pharmacy and Laboratory Medicine, Army Medical University, Shapingba, Chongqing 400038, China
- 2Department of Pharmacognosy, Faculty of Pharmacy and Laboratory Medicine, Army Medical University, Shapingba, Chongqing 400038, China
Abstract
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.
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BibTeX
@article{liu2026bupleurum,
title = {{Bupleurum chinense DC.–Derived Acidic Polysaccharide: Alleviates Lipopolysaccharide-Induced Acute Lung Injury via Activation of Siglec-E}},
author = {Yaoyao Liu and Juanjuan Liu and Jin Li and Hongmei Liu and Xiaodong Ran and Yan Huang and Yi Jia},
journal = {Molecules},
year = {2026},
month = nov,
doi = {10.3390/molecules31213989},
url = {https://www.mdpi.com/1420-3049/31/21/3989},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Bupleurum chinense DC.–Derived Acidic Polysaccharide: Alleviates Lipopolysaccharide-Induced Acute Lung Injury via Activation of Siglec-E
AU - Yaoyao Liu
AU - Juanjuan Liu
AU - Jin Li
AU - Hongmei Liu
AU - Xiaodong Ran
AU - Yan Huang
AU - Yi Jia
PY - 2026
DA - 2026/11/05
JO - Molecules
DO - 10.3390/molecules31213989
UR - https://www.mdpi.com/1420-3049/31/21/3989
AB - 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.
SN - 1420-3049
ER -