Erianin alleviates collagen-induced arthritis in mice by inhibiting Th17 cell differentiation.

Rheumatoid arthritis (RA) is a chronic autoimmune disorder. Its pathogenesis is complicated but highly related to aberrant Th17 overactivation. Uncontrolled Th17 cell expansion and activation in populations and associated activities contribute to the progression of RA. Although clinical RA remedies are available, not all RA patients respond to these treatments, and adverse effects are always a concerning issue during treatment. To expand the repertoire of possible anti-RA remedies, we chose the phytochemical compound erianin, isolated from sp., and evaluated its antiarthritic effect and . We found that erianin efficiently controlled the differentiation and activation of Th17 cell development from primary CD4 T cells, limiting IL-17A cytokine production and RORγT transcript generation. In line with molecular docking models, the essential signaling pathway for Th17 polarization, the JAK/STAT3 pathway, was inhibited upon erianin treatment, with dose-dependent inhibition of phosphorylation shown by western blotting. More importantly, erianin treatment reduced arthritic manifestations and proinflammatory cytokine levels in collagen-induced arthritis (CIA) mice, as well as protecting the joint histological microstructure. Overall, erianin revealed a promising inhibitory effect on Th17 overactivation and decreased disability in CIA mice. Therefore, erianin could be further developed as a candidate RA remedy.