【Animal Modeling】-How to study collagen-induced arthritis disease/syndrome model?

  Objective: To study the expression of serum cytokines in collagen-induced rheumatoid arthritis, cold-damp arthralgia and damp-heat arthralgia/syndrome model rats?

  Method: Rheumatoid arthritis uses bovine type II collagen and Freund's complete adjuvant. This model establishes a combined model of cold-damp arthralgia and damp-heat arthralgia syndrome by applying cold-damp-heat stimulation or damp-heat stimulation, and uses micro Array antibody chip detects the expression of serum cytokines.

  Results: In the RA group, activinA? CNTF? IFN-γ? TNF-α was controlled upward, MIP-3α? MMP-8 was controlled downward, and compared with the normal group, CINC-2α? GM-CSF was controlled by IFN-γ upward. MIP- 3α was inhibited in the cold-damp arthralgia group, ICAM-1 was up-regulated in the damp-heat joint pain group, β-NGF? CINC-2α? MMP-8? PDGF-AA was up-regulated, and activin? TNF-α was up-regulated in the cold-damp arthralgia group Moderate down regulation; MMP-8 up-regulated in damp-heat joint pain group, activin IL-1?IL-6? Cold and damp-inhibiting group heat ratio heat ratio group and MIP-3?RAGE?TNF-α downregulated A, CINC-2α? IFN -γ? IL-1α? MIP-3α? PDGF-AA "RAGE all up-regulated" Normal. Compared with the group, the ratio of IFN-γ/IL-4 increased. RA group and half-day group, the proportion of damp-heat joint pain group significantly decreased . A Compared with the two groups, does the proportion of cold-damp joint pain group increase, and does the proportion of damp-heat joint pain group decrease significantly?

  Conclusion: Is the disease/syndrome factor in the serum cytokine expression profile? It has a major impact. Is there a significant difference between the rat and the model?