ArticleDrug design, development and therapy2024
Sinomenine Alleviates Rheumatoid Arthritis by Suppressing the PI3K-Akt Signaling Pathway, as Demonstrated Through Network Pharmacology, Molecular Docking, and Experimental Validation.
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 13 papers, 1 of them a synthesis that pooled it.
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
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Sinomenine ameliorates rheumatoid arthritis in rodent models: a systematic review and meta-analysis of anti-inflammatory and joint-protective effects.Frontiers in pharmacology · 2026Pooled it
- Integrated LC-Orbitrap-MS and network pharmacology decipher the pharmacological basis of Eucommiae folium in treating rheumatoid arthritis.Molecular diversity · 2026Article
- Network Pharmacology Identifies IKBKB as the Primary Target of Sinomenine in Osteoarthritis, with Accuracy Benchmarking and Orthogonal Validation.Biomedicines · 2026Article
- Integrative Network Toxicology, Machine Learning, Single-Cell Analysis, scTenifoldKnk-Based Virtual Knockout, and Molecular Docking Suggest a Potential Molecular Link Between Aspartame and Rheumatoid Arthritis InvolvingInternational journal of molecular sciences · 2026Article
- Sinomenine ameliorates experimental autoimmune neuritis by suppressing pro-inflammatory immune components and restoring immune balance.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Bridging Pharmacology and Nanotechnology: Mechanistic Insights into Traditional Chinese Medicine-Based Nanodelivery Systems for Rheumatoid Arthritis.International journal of nanomedicine · 2026Review
- NR1D1-Mediated Suppression of JAK1/STAT3 Signaling Contributes to the Therapeutic Effects of Triptolide in Rheumatoid Arthritis.Mediators of inflammation · 2026Article
- Mechanisms of the Compound of Magnoliae Flos and Xanthii Fructus Essential Oils for the Treatment of Allergic Rhinitis based on the Integration of Network Pharmacology, Molecular Docking, and Animal Experiment.Combinatorial chemistry & high throughput screening · 2026Article
- B cell receptor signaling in autoimmune rheumatic diseases: regulatory mechanisms and therapeutic targeting.Frontiers in immunology · 2026Review
- Pharmacological Inhibition of the PI3K/AKT/mTOR Pathway in Rheumatoid Arthritis Synoviocytes: A Systematic Review and Meta-Analysis (Preclinical).Pharmaceuticals (Basel, Switzerland) · 2025Review
- Investigating the Mechanism of Action ofMarine drugs · 2025Article
- Suppression of Inflammation by Si Miao San in Experimental Rheumatoid Arthritis Through Modulation of the AKT/ROS/Autophagy Axis.Journal of inflammation research · 2025Article
- Research progress in treatment of rheumatoid arthritis with Sinomenine and related formulations based on different administration routes.Frontiers in pharmacology · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Sinomenine (SIN) is commonly used in Traditional Chinese Medicine (TCM) as a respected remedy for rheumatoid arthritis (RA). Nevertheless, the therapeutic mechanism of SIN in RA remains incompletely understood. This study aimed to delve into the molecular mechanism of SIN in the treatment of RA. Methods: The potential targets of SIN were predicted using the TCMSP server, STITCH database, and SwissTarget Prediction. Differentially expressed genes (DEGs) in RA were obtained from the GEO database. Enrichment analyses and molecular docking were conducted to explore the potential mechanism of SIN in the treatment of RA. In vitro and in vivo studies were conducted to validate the intervention effects of SIN on rheumatoid arthritis, as determined through network pharmacology analyses. Results: A total of 39 potential targets associated with the therapeutic effects of SIN in RA were identified. Enrichment analysis revealed that these potential targets are primarily enriched in PI3K-Akt signaling pathway, and the molecular docking suggests that SIN may act on specific proteins in the pathway. Experimental results have shown that exposure to SIN inhibits cytokine secretion, promotes apoptosis, reduces metastasis and invasion, and blocks the activation of the PI3K-Akt signaling pathway in RA fibroblast-like synoviocytes (RA-FLS). Moreover, SIN treatment alleviated arthritis-related symptoms and regulated the differentiation of CD4+ T cells in the spleen of collagen-induced arthritis (CIA) mice. Conclusion: By utilizing network pharmacology, molecular modeling, and in vitro/in vivo validation, this study demonstrates that SIN can alleviate RA by inhibiting the PI3K-Akt signaling pathway. These findings enhance the understanding of the therapeutic mechanisms of SIN in RA, offering a stronger theoretical foundation for its future clinical application.
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.