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Lycium barbarum polysaccharide attenuates Pseudomonas-aeruginosa pyocyanin-induced cellular injury in mice airway epithelial cells

berries have been utilized in Asia for many years. However, the mechanisms of its lung-defensive properties are indeterminate. We investigate whether polysaccharide (LBP) could weaken infection-induced lung injury. Mice primary air-liquid interface epithelial cultures were pretreated with LBP and su...

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Bibliographic Details
Published in:Food & nutrition research 2022-02, Vol.66, p.1-12
Main Authors: Lin, Xue, Song, Fuyang, Wu, Yiming, Xue, Di, Wang, Yujiong
Format: Article
Language:English
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Summary:berries have been utilized in Asia for many years. However, the mechanisms of its lung-defensive properties are indeterminate. We investigate whether polysaccharide (LBP) could weaken infection-induced lung injury. Mice primary air-liquid interface epithelial cultures were pretreated with LBP and subsequently treated with pyocyanin (PCN). Lung injury, including apoptosis, inflammation, and oxidative stress, was estimated by western blot, enzyme-linked immunosorbent assay, . Flow cytometry was used to test cell apoptosis. Moreover, Balb/c mice were used to evaluate the tissue injury. We used hematoxylin-eosin staining and immunofluorescence to detect the expression of related proteins and tissue damage in mouse lungs and spleen. The flow cytometric analysis shows the potential of LBP to reduce time-dependent cell death by PCN. Mechanistically, LBP reduces PCN-induced expression of proapoptotic proteins and caspase3 and induces the activation of Bcl-2 in mice bronchial epithelial cells. Similarly, LBP reduces PCN-induced intracellular reactive oxygen species (ROS) production. Moreover, LBP inhibits the production of inflammatory cytokines, Interleukin (IL-1β), Tumor Necrosis Factor ( , IL-6, and IL-8. Our study confirms the ability of LBP to retard PCN-induced injury in mice lung and spleen. The inhibition of PCN-induced lung injury by LBP is capable of protecting mice cells from injury.
ISSN:1654-661X
1654-661X
DOI:10.29219/fnr.v66.4585