Pakistan journal of pharmaceutical sciences · 2026
Bruceine A alleviates lung injury in sepsis-associated acute respiratory distress syndrome by modulating macrophage polarization and NF-κB pathway activity.
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Lv Jianlei, Wu Songbai, Liu Min, Huang Kang
Аннотация
BACKGROUND: Sepsis-associated acute respiratory distress syndrome (ARDS) is a severe inflammatory lung disorder with high mortality. Bruceine A (BA), a quassinoid from Brucea javanica, exhibits anti-inflammatory and immunomodulatory activities, but its role in ARDS is unclear.
OBJECTIVES: This study evaluated the protective effects of BA in lipopolysaccharide (LPS)-induced ARDS and explored its underlying mechanisms.
METHODS: Thirty-six C57BL/6 mice were randomized into four groups: Control, LPS, LPS+BA and LPS+dexamethasone (Dex). Lung injury was assessed by histopathology, wet/dry weight ratio and TUNEL assay. Cytokine levels (TNF-α, IL-6, IL-1β, IL-10) were measured by ELISA. Macrophage polarization markers (iNOS, COX-2, Arg-1, YM1, CD206) and NF-κB pathway proteins were evaluated using immunohistochemistry and Western blotting.
RESULTS: BA significantly alleviated LPS-induced lung injury, reducing edema, tissue damage and alveolar apoptosis. It suppressed proinflammatory cytokines while enhancing IL-10. BA shifted macrophage polarization from proinflammatory M1 toward anti-inflammatory M2 phenotypes. Furthermore, BA inhibited NF-κB activation, evidenced by reduced phosphorylated p65 and restored IκBα levels. These effects were comparable to Dex.
CONCLUSION: BA protects against LPS-induced ARDS in mice by modulating cytokine release, promoting M2 macrophage polarization and suppressing NF-κB activation. These findings suggest BA as a promising natural immunomodulatory agent for inflammatory lung diseases.
OBJECTIVES: This study evaluated the protective effects of BA in lipopolysaccharide (LPS)-induced ARDS and explored its underlying mechanisms.
METHODS: Thirty-six C57BL/6 mice were randomized into four groups: Control, LPS, LPS+BA and LPS+dexamethasone (Dex). Lung injury was assessed by histopathology, wet/dry weight ratio and TUNEL assay. Cytokine levels (TNF-α, IL-6, IL-1β, IL-10) were measured by ELISA. Macrophage polarization markers (iNOS, COX-2, Arg-1, YM1, CD206) and NF-κB pathway proteins were evaluated using immunohistochemistry and Western blotting.
RESULTS: BA significantly alleviated LPS-induced lung injury, reducing edema, tissue damage and alveolar apoptosis. It suppressed proinflammatory cytokines while enhancing IL-10. BA shifted macrophage polarization from proinflammatory M1 toward anti-inflammatory M2 phenotypes. Furthermore, BA inhibited NF-κB activation, evidenced by reduced phosphorylated p65 and restored IκBα levels. These effects were comparable to Dex.
CONCLUSION: BA protects against LPS-induced ARDS in mice by modulating cytokine release, promoting M2 macrophage polarization and suppressing NF-κB activation. These findings suggest BA as a promising natural immunomodulatory agent for inflammatory lung diseases.