Journal
JOURNAL OF THE CHINESE MEDICAL ASSOCIATION
Volume 82, Issue 3, Pages 202-208Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/JCMA.0000000000000029
Keywords
CIA mice; Dioscin; Th17; Treg; STAT
Categories
Funding
- National Natural Science foundation of China [81273986]
Ask authors/readers for more resources
Background: This study was conducted to investigate the treatment efficacies and immunological mechanisms of action of dioscin in mice with chicken collagen type II-induced arthritis (CIA). Methods: The CIA mice was randomly divided into the model group (M), dioscin group (D), and tripterygium group (T); a normal control group (C) was also included. Each group was orally administered with related drugs or an equal volume of solvent (group C) starting on the 21st day of primary immunity, after which the levels of T helper 17 cells (Th17), regulatory T cells (Tregs), and their related factors were detected on the 35th day. Results: Compared to group C, group M exhibited significantly increased levels of interleukin 17 (IL-17) and IL-6 and decreased IL-27 (p < 0.05). Group D exhibited significantly decreased levels of IL-17 and IL-6 compared with group M (p < 0.05). Group M showed a significantly increased ratio of Th17 cells (p < 0.05), while dioscin significantly reduced this ratio (p < 0.05). Groups M and C showed no significant difference in the ratio of Tregs (p > 0.05) but dioscin significantly increased this ratio (p < 0.05). Group M significantly increased signal transducer and activator of transcription 3 (STAT3) and STAT5 compared with that in group C (p < 0.05), while the T and D groups showed significantly reduced levels of STAT3 and STAT5 (p < 0.05). Conclusion: Dioscin may affect the differentiation of Th17 and Tregs and secretion of related factors by regulating CD4(+) T cell subset-related signal transduction and the expression of transcription-activating factor STAT3 and STAT5, thus exerting useful immunoregulatory roles in CIA mice.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available