Effects of Astragalus glycoprotein on Th17/Treg cells in mice with collagen-induced arthritis

Z H Wang, C Qin, T Ran, D Q Yang, J H Guo

Article ID: 5235
Vol 32, Issue 4, 2018
DOI: https://doi.org/10.54517/jbrha5235
Received: 8 September 2018; Accepted: 8 September 2018; Available online: 8 September 2018; Issue release: 8 September 2018

Abstract

In this study of Th17/Treg cells, the therapeutic effect of Astragalus glycoprotein on collagen-induced arthritis in mice (CIA) was explored, and a basis for the clinical treatment of rheumatoid arthritis is provided. Sixty mice were selected for the establishment of a CIA mouse model, and were then randomly divided into a CIA model group, a hydrocortisone control group, a low, medium, and high dose group of Astragalus glycoprotein, respectively. The same number of control groups with same number of mice was established and after basic immunization, intraperitoneal injections were given once daily for two weeks in the treatment. At the end of the treatment, the mice in each group were selected and the proportion of Th17/Treg cells was detected by flow cytometry. The expression and positive expression of RORt, Foxp3, P-STAT3 and P-STAT5 protein were detected by Western blot and immunohistochemistry. Astragalus glycoprotein was shown to potentially improve the diet and mental state, reduce the arthritis index score and improve the pathological state of synovial membranes in the mice. Moreover, flow cytometry results showed that, compared with the CIA model group, the proportion of Th17 cells in the four other groups of mice decreased, while the proportion of Treg cells increased. This difference was statistically significant (P less than 0.05). From the experiment, the following conclusions were drawn: Astragalus glycoprotein can reduce Th17 cells and their transcription factors in the peripheral blood of CIA mice, up-regulate Treg cells and their transcription factors, and correct the balance of Th17/Treg cells so as to achieve an effective of treatment for CIA mice.


Keywords

yellow glycoprotein;collagen-induced arthritis;Th17/Treg cells;transcription factors


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