ArticleOpen life sciences2024
BA inhibits LPS-stimulated inflammatory response and apoptosis in human middle ear epithelial cells by regulating the Nf-Kb/Iκbα axis.
Article in Open life sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- The study of JAZF1-mediated apoptosis of decidual stromal cells by activating the NF-κB signaling pathway in spontaneous preterm birth.BMC pregnancy and childbirth · 2025Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Otitis media (OM) is a prevalent childhood ear disease characterized by inflammation of the middle ear cavity, which can lead to ear pain, fever, and hearing loss. The pathogenesis of OM is multifaceted, encompassing a variety of factors including bacterial or viral infections, host immune responses, and the function of middle ear epithelial cells. Boswellic acid (BA), a natural triterpene compound extracted from frankincense resin, has been proven to possess significant anti-inflammatory and immunomodulatory effects. This study aims to investigate the effects of BA on lipopolysaccharide (LPS)-stimulated inflammatory responses and apoptosis in human middle ear epithelial cells (HMEECs) and its potential mechanisms. Our findings demonstrated that BA enhances the proliferation of LPS-stimulated HMEECs and concurrently inhibits their apoptosis. In addition, BA blocked LPS-stimulated HMEEC inflammation. Mechanistically, BA suppressed the NF-κB/IκBα axis in LPS-stimulated HMEECs. In conclusion, BA effectively inhibits LPS-stimulated inflammation and apoptosis by mediating the NF-κB/IκBα axis, highlighting its potential as a therapeutic agent for OM.
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Registered trials
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