Residential College | false |
Status | 已發表Published |
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 Publication | European Journal of Pharmacology |
ISSN | 0014-2999 |
Volume | 984Pages: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. |
Keyword | Tulipalin a Acute Lung Injury M1 Polarization Macrophage Dna Binding Activity Nf-κb |
DOI | 10.1016/j.ejphar.2024.177034 |
URL | View the original |
Indexed By | SCIE |
Language | 英語English |
WOS Research Area | Pharmacology & Pharmacy |
WOS Subject | Pharmacology & Pharmacy |
WOS ID | WOS:001332438200001 |
Publisher | ELSEVIER, RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS |
Scopus ID | 2-s2.0-85205931921 |
Fulltext Access | |
Citation statistics | |
Document Type | Journal article |
Collection | Institute of Chinese Medical Sciences |
Corresponding Author | Yu, Hua; Shen, Xiang Chun; Li, Hai Yang |
Affiliation | 1.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 Affilication | Institute 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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