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Tulipalin A suppressed the pro-inflammatory polarization of M1 macrophage and mitigated the acute lung injury in mice via interference DNA binding activity of NF-κB
Linghu, Ke Gang1,2; Tuo, Yue Ting1; Cui, Wen Qing1,3; Li, Tai Qin1; Wang, Da Song1; Zhang, Ya Ya1; Zhang, Jian1; Zhang, Tian2,3; Wang, Yu E.1,2; Yu, Hua1,3; Shen, Xiang Chun1; Li, Hai Yang2
2024-12-05
Source PublicationEuropean Journal of Pharmacology
ISSN0014-2999
Volume984Pages:177034
Abstract

Acute lung injury (ALI) is an inflammatory disorder accompanied by higher morbidity and mortality. The pathological mechanism of ALI has been reported to be associated with the release of inflammatory cytokines by macrophages. Sesquiterpene lactones (SLs) represent the principal anti-inflammatory components of many natural products. Tulipalin A is a natural small molecule and a conserved moiety in anti-inflammatory SLs. However, the anti-inflammatory potential of Tulipalin A has yet to be fully disclosed. The present study aims to investigate TulipalinA's anti-inflammatory activity and underlying mechanisms in vitro and in vivo. Tulipalin A suppressed inflammatory responses in lipopolysaccharide (LPS)-stimulated bone marrow-derived primary macrophages and ameliorated LPS-induced ALI in mice. Mechanistically, Tulipalin A directly targets the NF-κB p65 and disrupts its DNA binding activity, thereby impeding the activation of NF-κB. Inhibition of NF-κB attenuated M1 polarization of macrophages, consequently suppressing the production of pro-inflammatory mediators and ameliorating the onset and progression of ALI. These findings suggest Tulipalin A's potential to mitigate inflammatory disorders like ALI via targeting NF-κB p65 and disrupting its DNA binding activity.

KeywordTulipalin a Acute Lung Injury M1 Polarization Macrophage Dna Binding Activity Nf-κb
DOI10.1016/j.ejphar.2024.177034
URLView the original
Indexed BySCIE
Language英語English
WOS Research AreaPharmacology & Pharmacy
WOS SubjectPharmacology & Pharmacy
WOS IDWOS:001332438200001
PublisherELSEVIER, RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
Scopus ID2-s2.0-85205931921
Fulltext Access
Citation statistics
Document TypeJournal article
CollectionInstitute of Chinese Medical Sciences
Corresponding AuthorYu, Hua; Shen, Xiang Chun; Li, Hai Yang
Affiliation1.The Key Laboratory of Optimal Utilization of Natural Medicine Resources, School of Pharmaceutical Sciences, Guizhou Medical University, Guian New District, Guizhou, China
2.Guizhou Institute of Precision Medicine, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China
3.State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao SAR, China
Corresponding Author AffilicationInstitute of Chinese Medical Sciences
Recommended Citation
GB/T 7714
Linghu, Ke Gang,Tuo, Yue Ting,Cui, Wen Qing,et al. Tulipalin A suppressed the pro-inflammatory polarization of M1 macrophage and mitigated the acute lung injury in mice via interference DNA binding activity of NF-κB[J]. European Journal of Pharmacology, 2024, 984, 177034.
APA Linghu, Ke Gang., Tuo, Yue Ting., Cui, Wen Qing., Li, Tai Qin., Wang, Da Song., Zhang, Ya Ya., Zhang, Jian., Zhang, Tian., Wang, Yu E.., Yu, Hua., Shen, Xiang Chun., & Li, Hai Yang (2024). Tulipalin A suppressed the pro-inflammatory polarization of M1 macrophage and mitigated the acute lung injury in mice via interference DNA binding activity of NF-κB. European Journal of Pharmacology, 984, 177034.
MLA Linghu, Ke Gang,et al."Tulipalin A suppressed the pro-inflammatory polarization of M1 macrophage and mitigated the acute lung injury in mice via interference DNA binding activity of NF-κB".European Journal of Pharmacology 984(2024):177034.
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