ArticleInflammopharmacology2019
Ginsenoside compound-K inhibits the activity of B cells through inducing IgD-B cell receptor endocytosis in mice with collagen-induced arthritis.
Article in Inflammopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 25 citations in OpenAlex.
- Ginsenoside CK potentiates SIRT1 to alleviate lupus nephritis through compensating for XBP1-mediated endoplasmic reticulum stress in plasma cells.Journal of pharmaceutical analysis · 2025Article
- Ginsenoside C-K inhibits Aβ oligomer-induced Alzheimer's disease pathology progression by regulating microglia-neuron interactions.IBRO neuroscience reports · 2025Article
- CXCL7 enhances RANKL-induced osteoclastogenesis via the activation of ERK/NFATc1 signaling pathway in inflammatory arthritis.Arthritis research & therapy · 2025Article
- Rare ginsenosides: A unique perspective of ginseng research.Journal of advanced research · 2024Review
- Triterpenes as Potential Drug Candidates for Rheumatoid Arthritis Treatment.Life (Basel, Switzerland) · 2023Review
- Regulating Th17/Treg Balance Contributes to the Therapeutic Effect of Ziyuglycoside I on Collagen-Induced Arthritis.International journal of molecular sciences · 2022Article
- A narrative review of the pharmacology of ginsenoside compound K.Annals of translational medicine · 2022Review
- Natural medicines of targeted rheumatoid arthritis and its action mechanism.Frontiers in immunology · 2022Review
- Combination therapy of ginsenoside compound K and methotrexate was efficient in elimination of anaemia and reduction of disease activity in adjuvant-induced arthritis rats.Pharmaceutical biology · 2020Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previously, ginsenoside metabolite compound K (C-K) was able to reduce B cell proliferation and serum anti-type II collagen (anti-CII) antibody to normal levels in mice with collagen-induced arthritis (CIA); however, the mechanism by which C-K restores B cell balance is unclear. In the present work, C-K treatment not only alleviated the polyarthritis index, swollen joint count, pathological scores of spleen and joints, spleen index, B cell proliferation and the level of serum antibodies (IgG1, IgG2a and anti-collagen II), but C-K treatment also restored B cell subsets including regulatory B cells, plasma cells, memory B cells, mature B cells, and follicular B cells in CIA mice. Interestingly, C-K did not change the expression level of immunoglobulin D-type B-cell receptor (IgD-BCR) but promoted IgD-BCR endocytosis. C-K treatment enhanced β-arrestin1 expression, facilitating the colocalization between IgD and β-arrestin1, as well as colocalization between IgD and adaptor protein 2 (AP2). Inhibition of the β-arrestin1-AP2 interaction with barbadin significantly reduced the ability of C-K to attenuate IgD-BCR plasma membrane localization. These results taken together depict that C-K ameliorates CIA in part by inhibiting B cell activation through the triggering of IgD-BCR internalization in a β-arrestin1-AP2 dependent manner.
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