ArticleScientific reports2025
NOTCH pathway was involved in Kaempferol 3-O-gentiobioside attenuated airway inflammation and mucus hypersecretion.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Flavonoids as Nutraceuticals to Treat Inflammatory Diseases: Focusing on Quercetin, Kaempferol, Luteolin, Apigenin, Epicatechin and Their Effects on Hepatic, Nervous, and Pulmonary Systems.Foods (Basel, Switzerland) · 2026Review
- Drug target mining and in silico screening of Tibetan plant metabolites for potential alleviation of Oroya fever, a neglected tropical disease.Scientific reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Allergic asthma is an inflammatory condition characterized by the release of pro-inflammatory cytokines and the expansion of mucus-producing cells. This research aimed to evaluate the impact of Kaempferol 3-O-gentiobioside (K3G), extracted from Sauropus spatulifolius Beille leaves, on inflammatory cytokine secretion and mucus overproduction in IL-13-stimulated airway epithelial cells (16HBE cells) and ovalbumin (OVA)-induced allergic asthma mouse models. Studies have found that K3G significantly reduces the release of pro-inflammatory cytokines (IgE, TNF-α, histamine, IL-1β, IL-6, and IL-8) induced by IL-13. It also mitigating the expression of the mucin5AC (MUC5AC). Additionally, K3G also downregulated the expression of NLRP3, TLR4, p-IκBα, and p-P65 proteins. In an OVA-induced mouse asthma model, K3G treatment reduced the secretion of pro-inflammatory cytokines, and inhibited the increase in mucus-secreting cells in a dose-dependent manner. Furthermore, exposure to IL-13 and OVA increased the expression of NOTCH signaling receptors in both 16HBE cells and lung tissues of the mice. K3G treatment effectively targeted NOTCH1 and inhibits activation of the NOTCH pathway. In conclusion, K3G alleviates asthma-related airway alterations by suppressing inflammatory cytokines and excessive mucus secretion via the NOTCH signaling pathway. These results indicate the therapeutic promise of K3G in treating allergic asthma.
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.