ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Revealing the bioactive components and possible mechanism of Tongbi Lingding in the treatment of osteoarthritis based on UPLC-MS/MS, network pharmacology, transcriptomics, molecular docking, and experimental validation.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. 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
10 authors.
Funding
Abstract
Tongbi Lingding (TBLD) has demonstrated therapeutic effects in early- and mid-stage osteoarthritis (OA), but its active components and underlying mechanisms remain unclear. This study aimed to identify the bioactive compounds of TBLD and explore the potential molecular mechanisms underlying its therapeutic effects against OA. A destabilization of the medial meniscus (DMM)-induced OA mouse model and IL-1β-stimulated chondrocytes were used to evaluate the therapeutic effects of TBLD. Ultra-performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS/MS) was performed to identify TBLD-associated compounds in blood and knee joints. Network pharmacology, transcriptomic analysis, molecular docking, and in vitro experiments were integrated to investigate the potential mechanisms underlying the effects of TBLD. TBLD markedly alleviated cartilage degeneration and subchondral bone sclerosis in OA mice. UPLC-MS/MS identified 2295 compounds, among which 178 and 102 TBLD-associated compounds were detected in blood and knee joints, respectively. Seventy-six compounds with predicted targets and 153 shared targets were identified. Functional enrichment analysis indicated that these targets were mainly associated with the NOD-like receptor (NLR) and NF-κB signaling pathways. Molecular docking predicted potential interactions between key compounds and NLRP3 and p65. Furthermore, hinokiflavone and dehydroabietic acid suppressed inflammatory responses, restored extracellular matrix metabolism, and inhibited IL-1β-induced MMP3 and MMP13 expression in chondrocytes. Hinokiflavone treatment also reduced the expression of NLRP3 inflammasome-related proteins and attenuated the phosphorylation of NF-κB signaling-related proteins in TNF-α-stimulated chondrocytes. TBLD exerts protective effects against OA that may be associated with changes in NLRP3/NF-κB-related inflammatory signaling, further supporting its potential therapeutic application in OA.
Indexed as
Identifiers
42760374What 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.