Objective: To explore the therapeutic effect and possible mechanism of Huangqi glycoprotein (HQGP) on the development of experimental autoimmune encephalomyelitis (EAE).
Methods: Female C57BL/6 mice were immunized subcutaneously with myelin oligodendrocyte glycoprotein peptide-35-55 (MOG35-55) and divided into HQGP-treated group and EAE control group. Clinical score and body mass were recorded every other day. Inflammatory cell infiltrations of spinal cord were observed by HE and immunofluorescence staining. The cell viability of splenic mononuclear cells (MNCs) was detected by MTT assay. The release of NO was measured by Griess method. The levels of TNF-α, IL-6 and IFN-γ were determined by ELISA. The subtypes of CD4(+)T cells were analyzed by flow cytometry.
Results: HQGP treatment delayed the onset of EAE, attenuated the clinical symptoms and inhibited CD68(+) macrophage infiltration into the central nervous system. HQGP inhibited the viability of splenic MNCs, downregulated the secretion of NO, TNF-α, IL-6, and increased the secretion of IFN-γ. In addition, HQGP treatment effectively increased the numbers of CD4(+)CD25(+) T cells, CD4(+)IL-10(+) T cells and CD4(+)IFN-γ(+) T cells.
Conclusion: HQGP relieve the inflammation of EAE via reducing the number of T cell subsets and inhibiting the secretion of inflammatory cytokines.