ArticleScientific reports2025
Cepharanthine alleviates lipopolysaccharide-induced acute lung injury through modulating macrophage polarization.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Acute lung injury (ALI) is a common, severe respiratory disorder frequently related to acute lung inflammation. As crucial immunoregulatory cells, macrophages critically influence the pathological trajectory of ALI, with their functional states serving as predictive biomarkers for both lesion severity and patient recovery trajectories. Cepharanthine (CEP), a natural bisbenzylisoquinoline (BBIQ) alkaloid, was shown to have substantial anti-inflammatory properties. However, whether CEP can alleviate ALI by regulating macrophage polarization needs to be clarified. Therefore, the therapeutic effect of CEP in ALI was explored via H&E staining, enzyme-linked immunosorbent assays (ELISAs), immunofluorescence, and western blot. In vivo, experimental data demonstrated that CEP intervention significantly ameliorated mouse pathological alterations. Specifically, the secretion levels of pro-inflammatory cytokines IL-6 and TNF-α were dose-dependently downregulated, while the expression of the anti-inflammatory mediator IL-10 exhibited a significant upregulation trend. Immunofluorescence staining revealed that CEP suppressed lipopolysaccharide (LPS)-induced M1 macrophage polarization and increased M2 macrophage polarization. Moreover, western blot results showed that CEP inhibited TLR4/MAPK signaling pathway activation but increased AMPK phosphorylation and Nrf2/HO-1 expression. Experimental findings from in vitro studies aligned with observations corresponding to in vivo models. In summary, CEP can regulate macrophage polarization to protect against LPS-induced ALI by interfering with TLR4/MAPK signaling and activating the AMPK/Nrf2 pathway.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.