ArticleJournal of microbiology and biotechnology2025
Casticin Inhibits Osteoclastogenesis via NF-κB/BCL-2 Signaling Pathway.
Article in Journal of microbiology and biotechnology, 2025. 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
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
1 citing paper in PubMed.
- Casticin Alleviates Acetaminophen-Induced Acute Liver Injury by Modulating the TLR4/MyD88/TRAF6/NF-κB Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigates the effects of casticin on osteoclastogenesis, aiming to elucidate its underlying mechanisms for potential clinical applications. We assessed the cytotoxicity of casticin using a CCK assay in RAW 264.7cell (murine cell line, from ATCC), which differentiate into osteoclasts upon RANKL treatment. Various concentrations (0.125, 0.25, 0.50 μM) were tested to establish a dose-dependent response. The effects of casticin on osteoclast differentiation and actin filament organization were evaluated through TRAP and F-actin staining. Additionally, qPCR and Western blot analyses were performed to assess gene expression. Concentrations exceeding 1.00 μM caused significant cytotoxicity. Notably, casticin at 0.50 μM significantly inhibited osteoclast differentiation and function, reducing marker gene expression, including c-FOS, NFATc1, CtsK, and MMP-9. Furthermore, casticin decreased phosphorylation levels of NF-κB and IκBα and downregulated BCL-2 expression. Our findings highlight casticin's potent regulatory effects on osteoclasts via the NF-κB/BCL-2 signaling pathways, suggesting potential therapeutic applications in bone-related disorders.
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.