Oroxin B prevented sepsis-evoked acute lung injury by promoting M2 macrophage polarization through the TLR4/NF-κB axis

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dc.contributor.authorJianhua Liu
dc.contributor.authorChanghong Zhang
dc.contributor.authorFeng Li
dc.contributor.authorNana Duan
dc.contributor.authorZhihua Zhang
dc.contributor.authorChen Li
dc.contributor.departmentBiología Celular e Histología
dc.date.accessioned2025-11-11T09:25:40Z
dc.date.available2025-11-11T09:25:40Z
dc.date.issued2025
dc.description.abstractAcute lung injury (ALI) is a frequent complication of sepsis that aggravates sepsis mortality and morbidity, which is tightly related to the inflammatory process. Oroxin B (OB), a flavonoid from Oroxylum indicum (L.) Vent, has exhibited anti-inflammatory properties in several illnesses. Nevertheless, it is still unclear how OB affects sepsis-induced ALI and how it works. RAW264.7 cells were challenged with lipopolysaccharide (LPS, 10 μg/mL), and mice received cecal ligation and puncture (CLP) to produce sepsis-evoked ALI in in vitro and in vivo models. The action of OB on sepsis-elicited ALI was probed through cell counting kit-8, pathological staining, enzyme-linked immunosorbent assay, reverse transcription-quantitative polymerase chain reaction, and western blot. The results showed that OB improved pathological damage and pulmonary fibrosis in CLP-challenged mice. OB also reduced the concentration of MPO, the protein content in BALF, and macrophage and neutrophil numbers in BALF from CLP-challenged mice. Molecularly, OB decreased the levels of IL-1β, IL-6, TNF-α, CD86, and iNOS but increased the level of Arg1 and CD206 in both LPS-evoked RAW264.7 cells and CLP-treated mice. Mechanistically, OB downregulated the level of the TLR4/NF-κB axis in both LPS-challenged RAW264.7 cells and CLP-treated mice. Overexpression of TLR4 abrogated the effect of OB on the above-mentioned indicators in LPS-elicited RAW264.7 cells. Therefore, OB improved sepsis-elicited ALI by attenuating inflammation and promoting M2 macrophage polarization through the TLR4/NF-KB signaling pathway.
dc.formatapplication/pdf
dc.format.extent12
dc.identifier.doihttps://doi.org/10.14670/HH-18-916
dc.identifier.eissn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/172189
dc.languageeng
dc.relationSin financiacion externa a la Universidad
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectAcute lung injury
dc.subjectOroxin B
dc.subjectInflammation
dc.subjectMacrophage polarization
dc.subjectTLR4/NF-κB
dc.subjectSepsis
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleOroxin B prevented sepsis-evoked acute lung injury by promoting M2 macrophage polarization through the TLR4/NF-κB axis
dc.typeinfo:eu-repo/semantics/article
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Histology and histopathology, Vol.40, Nº12, (2025)