Open AccessBaicalin attenuates collagen‐induced arthritis via inhibition of JAK2‐STAT3 signaling and regulation of Th17 cells in mice
Author(s) -
Sun Fengchun,
Gu Wenjing
Publication year - 2018
Publication title -
journal of cell communication and signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 44
eISSN - 1873-961X
pISSN - 1873-9601
DOI - 10.1007/s12079-018-0475-1
Subject(s) - baicalin , arthritis , splenocyte , collagen induced arthritis , flow cytometry , medicine , stat3 , pharmacology , tumor necrosis factor alpha , immunology , signal transduction , chemistry , spleen , biochemistry , high performance liquid chromatography , chromatography
This study focused on the potential therapeutic effect of Baicalin on collagen‐induced arthritis (CIA) in mice and the underlying mechanisms. Baicalin (200 mg/kg) was administrated after the induction of CIA for 42 days. Therapeutic effects were evaluated by arthritic scores, X‐rays and assessment of histopathological joint destruction. The production of TNF‐α,IL‐6,IL‐17,IL‐1β were also measured. The percentage of Th17 cells in splenocytes were determined by flow cytometry analysis. Our results showed that Baicalin treatment attenuated the severity of arthritis of CIA mice and reduced the levels of several cytokines. Further mechanistic investigations revealed that Baicalin suppressed the expression and phosphorylation of JAK2 and STAT3 protein in splenocytes tissue. Moreover, the percentage of Th17 cells in splenocytes also downregulated by Baicalin. Our experiment indicate that CIA mice can be alleviated by Baicalin treatment via inhibition of JAK2‐STAT3 signaling and regulation of Th17 cells in mice.