Authors
Yan Jiang, Yuhu Feng, Xinyu Li, Bing Zhao, Zuisu Yang, Ruling Wei, Falei Yuan
Published in
PloS one. Volume 21. Issue 8. Pages e0356781. Epub Aug 26, 2026.
Abstract
This study examined the role of bovine serum albumin (BSA) in lipopolysaccharide (LPS)-induced brain injury. Mice were intraperitoneally injected with either LPS or LPS coupled with BSA. Brain tissues were analyzed for autofluorescence, vascular cell permeability, blood-brain barrier integrity, and pyroptosis. Co-immunoprecipitation and immunostaining were performed to assess the interaction between albumin and LPS. The results showed that, compared to the 5 mg/kg LPS group, the 5 mg/kg BSA-LPS group exhibited enhanced autofluorescence and an increased number of cells with co-localization of propidium iodide (PI) with cluster of differentiation 31 (CD31) and CD13. However, no significant differences were observed between the 25 mg/kg LPS and 25 mg/kg BSA-LPS groups. Horseradish peroxidase (HRP) labeling revealed higher HRP leakage in the 5 mg/kg BSA-LPS group compared to the 5 mg/kg LPS group, a difference that disappeared at the 25 mg/kg dose. Peroxidase staining showed a similar trend. Immunostaining for gasdermin D and CD11b showed significant differences only between the 5 mg/kg LPS and 5 mg/kg BSA-LPS groups. CD68 immunostaining exhibited a similar trend. Furthermore, the study confirmed that albumin binds to LPS in the brain, with more abundant Lipid A+ signals detected in the 5 mg/kg BSA-LPS group compared to the 5 mg/kg LPS group. These findings collectively suggest that albumin boosts the effect of LPS in the brain, probably by binding with LPS and increasing its entry into the brain parenchyma.
PMID:
42647552
Bibliographic data and abstract were imported from PubMed on 27 Aug 2026.
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