ArticleMolecular medicine reports2021
Ginkgolide J protects human synovial cells SW982 via suppression of p38‑dependent production of pro‑inflammatory mediators.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Serum Pharmacochemistry-Guided DARTS-MS Profiling Reveals Potential Mechanisms ofInternational journal of molecular sciences · 2026Article
- Study of the pharmacokinetics of Ginkgolide J in rats by ultra-high-performance liquid chromatography tandem mass spectrometry.Annals of medicine and surgery (2012) · 2026Article
- Synthesis, characterization andNanoscale advances · 2025Article
- Synovial Organoids and Cell Culture Models: An Ideal Platform for Exploring Traditional Chinese Medicine in Rheumatoid Arthritis.ACS omega · 2025Review
- A new 3-arylbenzofuran derivative EIE-2 reestablishes Treg-dependent tolerance in rheumatoid arthritis by targeting on Syk induced mTOR and PKCθ imbalance.Frontiers in immunology · 2025Article
- Regulating the lncRNA DSCR9/RPLP2/PI3K/AKT axis: an important mechanism of Xinfeng capsules in improving rheumatoid arthritis.Frontiers in immunology · 2024Article
- Study on Synergistic Anti-Inflammatory Effect of Typical Functional Components of Extracts of Ginkgo Biloba Leaves.Molecules (Basel, Switzerland) · 2023Article
- [Effects of serum fromNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast‑like synoviocytes (FLS) in the synovial lining play a key role in the pathological process of rheumatoid arthritis (RA), which produce pro‑inflammatory mediators to perpetuate inflammation and proteases to contribute to cartilage destruction. Ginkgolide J (GJ) is a subclass of ginkgolides (GGs) that exhibits anti‑inflammatory activity. In the present study, the protective effect of GJ on lipopolysaccharide (LPS)‑treated human synovial cells SW982 and its related mechanisms were investigated using various methods, including ELISA, Griess assay, western blotting, immunofluorescence analysis and p38 kinase activity assay. The results revealed that GJ pretreatment significantly attenuated LPS‑induced excess production of pro‑inflammatory mediators in SW982 cells via suppression of tumor necrosis factor‑α/interleukin (IL)‑1β/IL‑18/NF‑κB/NLR family pyrin domain containing 3, prostaglandin E2/cyclooxygenase‑2 and inducible nitric oxide synthase/nitric oxide signaling. Mechanistic studies revealed that p38 activation contributed to the LPS‑induced inflammatory response, and GJ pretreatment dose‑dependently attenuated p38 activation, indicating that the suppressive effect of GJ was achieved by targeting p38 signaling. These findings may contribute to the prevention and treatment of RA.
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