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Ginsenoside compound K suppresses the abnormal activation of T lymphocytes in mice with collagen-induced arthritis
Kang-kang Liu1, Qing-tong Wang1, Si-min Yang1
1Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine (Anhui Medical University), Ministry of Education, Hefei 230032, China.
Aim:
To investigate the anti-arthritis and immunomodulatory activities of ginsenoside compound K (C-K) in mice with collagen-induced arthritis (CIA).
Methods:
DBA/1 mice with CIA were treated with C-K (28, 56 or 112 mg·kg(-1)·d(-1), ig) or the positive control methotrexate (2 mg/kg, ig, every 3 d) for 34 d. Splenic T and B lymphocytes were positively isolated using anti-CD3-coated magnetic beads or a pan B cell isolation kit. T lymphocyte subsets, and CD28, T cell receptor (TCR), cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) and programmed death-1 (PD-1) expression in purified splenic T lymphocytes were analyzed using flow cytometry, Western blotting and laser confocal microscopy.
Results:
C-K treatment significantly ameliorated the pathologic manifestations of CIA mice, remarkably inhibited T lymphocyte proliferation, and marginally inhibited the proliferation of B lymphocytes. C-K treatment significantly suppressed TNF-α and anti-CII antibody levels, and increased IFN-γ level in the joints of CIA mice, but did not alter IL-4 production. Treatment of CIA mice with C-K significantly decreased the percentages of activated T cells, co-stimulatory molecule-expressing T cells and effector memory T cells, and increased the frequencies of naive T cells and regulatory T cells. Furthermore, C-K treatment significantly decreased the expression of CD28 and TCR, whereas it increased the expression of CTLA-4 and PD-1 on T lymphocytes of CIA mice. Methotrexate treatment exerted comparable effects in all these experiments.
Conclusion:
C-K suppresses the progression of CIA through regulating TCR, CD28, CTLA-4 and PD-1 expression, thus inhibiting the abnormal activation and differentiation of T lymphocytes.
Insights
Ginsenoside compound K (C-K) effectively treats collagen-induced arthritis (CIA) in mice by modulating T lymphocyte activity and immune responses. This natural compound shows promise for managing autoimmune arthritis.
Area of Science:
- Immunology
- Pharmacology
- Natural Products
Background:
- Collagen-induced arthritis (CIA) is a mouse model for rheumatoid arthritis, characterized by autoimmune responses.
- Ginsenoside compound K (C-K), a metabolite of ginsenosides, has shown potential anti-inflammatory properties.
Purpose of the Study:
- To investigate the anti-arthritis and immunomodulatory effects of C-K in a CIA mouse model.
- To elucidate the mechanisms by which C-K impacts T lymphocyte subsets and immune markers.
Main Methods:
- DBA/1 mice with CIA were treated with varying doses of C-K or methotrexate.
- Splenic T and B lymphocytes were isolated and analyzed for proliferation, subset distribution, and expression of key surface molecules (CD28, TCR, CTLA-4, PD-1).
- Cytokine levels (TNF-α, IFN-γ, IL-4) and antibody production were assessed.
Main Results:
- C-K treatment significantly reduced CIA pathology, T lymphocyte proliferation, and pro-inflammatory cytokine TNF-α.
- C-K modulated T cell populations, decreasing activated and effector memory T cells while increasing naive and regulatory T cells.
- Expression of CD28 and TCR was decreased, while CTLA-4 and PD-1 expression was increased on T lymphocytes.
Conclusions:
- C-K demonstrates significant anti-arthritis effects in CIA mice.
- The immunomodulatory activity of C-K involves the regulation of T lymphocyte activation and differentiation via TCR, CD28, CTLA-4, and PD-1 pathways.
