Baicalin Inhibits IL-17-Mediated Joint Inflammation in Murine Adjuvant-Induced Arthritis

Abstract EN

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.