ArticleImmunity, inflammation and disease2024
The SRC/NF-κB-AKT/NOS3 axis as a key mediator of Kaempferol's protective effects against oxidative stress-induced osteoclastogenesis.
Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Formononetin attenuates glucocorticoid-induced osteoporosis via multiple osteoimmunological pathways: evidence from zebrafish and network pharmacology.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026Article
- Targeting neuroimmune interactions: the therapeutic potential of kaempferol in immune-related central nervous system disorders.Frontiers in immunology · 2026Review
- The SRC/NF-κB-AKT/NOS3 axis as a key mediator of Kaempferol's protective effects against oxidative stress-induced osteoclastogenesis.Immunity, inflammation and disease · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundOsteoclasts are integral to the advancement of osteoporosis (OP), and their generation under conditions of oxidative stress (OS) involves various pathways. However, the specific mechanism through which the natural antioxidant kaempferol (KAE) mitigates the influence of OS on osteoclasts remains somewhat uncertain. This study aims to evaluate the effect of KAE on osteoclast formation under OS and explore its possible mechanism.
methodsZebrafish were used to observe the effects of KAE on OP and OS. OP and OS "double disease targets" network pharmacology were used to predict the action target and mechanism of KAE on OP under OS. The effects of KAE on osteoclast differentiation induced by OS were evaluated using RWA264.7 cells induced by LPS. To elucidate the potential mechanism, we detected the expression of related factors and target genes during induction.
resultsThe presence of KAE exhibited potential in improving the conditions of OP and OS in zebrafish. KAE can reduce the OS of RAW 264.7 cells stimulated by LPS, inhibit the formation of osteoclasts, and change the level of related factors of OS, and reduce the increase of TRAP. The utilization of network pharmacology and target gene expression assay revealed that KAE exerted a down-regulatory effect on the expression of proto-oncogene tyrosine protein kinase (SRC), nuclear factor kappa-B (NF-κB), Serine/Threonine Kinase-1 (AKT1), Nitric Oxide Synthase 3 (NOS3) and Matrix Metallopeptidase-2 (MMP2).
conclusionBased on the results of this study, KAE may effectively mitigate OS and impede the formation of osteoclasts through the SRC/NF-κB-AKT/NOS3 axis.
Indexed as
Identifiers
What Socratic 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 Socratic graph.