T-helper-17 (Th17) cells are implicated in a number of inflammatory disorders including rheumatoid arthritis. Antagonism of Th17 cells is a treatment option for arthritis. Here, we report that Baicalin, a compound isolated from the Chinese herb Huangqin (Scutellaria baicalensis Georgi), relieved ankle swelling and protected the joint against inflammatory destruction in a murine adjuvant-induced arthritis model. Baicalin inhibited splenic Th17 cell population expansion in vivo. Baicalin prevented interleukin- (IL-) 17-mediated lymphocyte adhesion to cultured synoviocytes. Baicalin also blocked IL-17-induced intercellular adhesion molecule 1, vascular cell adhesion molecule 1, IL-6, and tumor necrosis factor-alpha mRNA expression in cultured synoviocytes. Collectively, these findings suggest that Baicalin downregulates the joint inflammation caused by IL-17, which is likely produced by an expanded population of splenic Th17 cells in experimental arthritis. Baicalin might be a promising novel therapeutic agent for treating rheumatoid arthritis in humans.
Keyphrases
- rheumatoid arthritis
- induced apoptosis
- oxidative stress
- cell adhesion
- diabetic rats
- high glucose
- cell cycle arrest
- disease activity
- endothelial cells
- early stage
- interstitial lung disease
- stem cells
- endoplasmic reticulum stress
- cell proliferation
- signaling pathway
- systemic lupus erythematosus
- pseudomonas aeruginosa
- biofilm formation
- immune response
- cell migration
- smoking cessation
- regulatory t cells
- idiopathic pulmonary fibrosis
- bone marrow
- stress induced