Oroxin B prevented sepsis-evoked acute lung injury by promoting M2 macrophage polarization through the TLR4/NF-κB axis.
Year: 2025
Type: article
Abstract: 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.
Source: PubMed
DOI: 10.14670/hh-18-916
Authors: Chen Li, Jianhua Liu, Changhong Zhang, Feng Li, Nana Duan, Zhihua Zhang
Institution: Hebei North University
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W4409734703