ArticleDrug design, development and therapy2024
The Therapeutic Potential of Pristimerin in Osteoarthritis: Mechanistic Insights from in vitro and in vivo Studies.
Article in Drug design, development and therapy, 2024. 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
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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.
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Who cites it
2 citing papers in PubMed.
- Targeting the osteoimmune microenvironment to prevent regulated chondrocyte death in osteoarthritis: therapeutic potential of natural products.Frontiers in cell and developmental biology · 2026Review
- Triterpenoid Compounds and their Derivatives: Emerging Pharmacological Agents for Arthritis Treatment.Mini reviews in medicinal chemistry · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Osteoarthritis (OA), a degenerative disease marked by cartilage erosion and synovial proliferation, has led to an increased interest in natural plant-based compounds to slow its progression. Pristimerin(Pri), a triterpenoid compound derived from Tripterygium wilfordii, has demonstrated anti-inflammatory and antioxidant characteristics. This study explores the protective effects of Pri on OA and its potential mechanisms. Methods: In this study, we examined the impact of Pri on the expression of inflammatory factors and extracellular matrix(ECM) degradation induced by IL-1β in chondrocyte experiments. Bioinformatics analysis was then performed to investigate the potential signaling pathways involved in Pri's protective effects. Finally, the efficacy of Pri in reducing cartilage degradation was further evaluated in a destabilization of the medial meniscus (DMM) mouse model. Results: Utilizing bioinformatics analysis and in vitro studies, it was revealed that Pri inhibits the activation of NF-κB and MAPK signaling pathways, leading to the reversal of upregulated MMP-13 (matrix metalloproteinases-13), iNOS (inducible nitric oxide synthase), and COX-2(cyclooxygenase-2) elicited by IL-1β stimulation, as well as the partial restoration of Collagen-II levels. Furthermore, in a DMM mouse model, the group treated with Pri exhibited reduced cartilage degradation and slowed OA progression compared to the modeling group. Conclusion: This research highlights Pri as a potential therapeutic agent for delaying OA progression.
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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.