Suppressive Effects of GHS in Knee Joint, Regional Lymph Nodes, and Spleen on Collagen-induced Arthritis in Mice

Collagen II로 유도된 CIA 관절염 생쥐의 대한 가미해동피산(加味海桐皮散)의 억제 효과

  • Kim, Nam-Uk (Department of Pathology, College of Oriental Medicine, Daejeon University) ;
  • Kim, Dong-Hui (Department of Pathology, College of Oriental Medicine, Daejeon University)
  • 김남욱 (대전대학교 한의과대학 병리학교실) ;
  • 김동희 (대전대학교 한의과대학 병리학교실)
  • Published : 2007.10.25

Abstract

Rheumatoid arthritis (RA) is a systemic autoimmune disease with chronic inflammation characterized by hyperplasia of synovial cells in affected joints, which might be mediated by the altered activation of Immune system, ultimately leading to the destruction of cartilage and bone. To examine effects of GHS on rheumatoid arthritis DBA/1J mice were immunized with bovine type II collagen to induced arthritis and then treated with GHS once a day for 7 weeks. Oral administration of GHS (200 mg/Kg) significantly suppressed the progression of CIA, which extend is comparable to that of methotrexate (MTX, 0.3 mg/Kg), a positive control. The severity of arthritis within the knee joints, which was evaluated by histological assessment of cartilage destruction and pannus formation, was also lowered by GHS. The production of TNF-and IL-6 in serum was significantly suppressed. The levels of IFN-g in the culture supernatant of splenocytes stimulated with CD3/CD28 or collagen were dramatically decreased, while those of IL-4 was increased. The levels of IgG and IgM RA factor were also decreased in the serum. FACS analysis indicated that B cells (in DLN), CD3+ T cells (in spleen, and paw joint), CD11b+Gr-1+ cells (in paw joint), CD3+CD49b(DX5) (in PBMC) were decreased and there was increased proportion of CD3+, CD4+, CD8+, CD4+CD25+ T cells in DLN. In conclusion, our results demonstrates that GHS significantly suppressed the progression of CIA and this action was characterized by the decreased production of TNF-a, IL-6, and rheumatoid factors, and modulations of immune cell populations.

Keywords

References

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