Significance: Bile acids bind to the nuclear hormone receptor, farnesoid X receptor (FXR). This bile acid–FXR interaction regulates bile acid synthesis, transport, and cholesterol metabolism. Recently, drugs targeting FXR activation have been reported to treat both liver and intestinal inflammatory diseases in both animal models and human clinical trials. Experimental autoimmune encephalomyelitis (EAE) is an inflammatory demyelinating disease of the central nervous system and serves as an animal model for multiple sclerosis (MS). In this study, we found that FXR knockout mice had more severe EAE, and treatment of mice with established EAE with a synthetic FXR agonist, obeticholic 
acid (6α-ethyl-Chenodeoxycholic Acid, 6-ECDCA), reduced EAE severity. Thus, we provide an FXR target for development of a previously unidentified disease-modifying therapy for MS.
Bile acids are ligands for the nuclear hormone receptor, farnesoid X receptor (FXR). The bile acid–FXR interaction regulates bile acid synthesis, transport, and cholesterol metabolism. Recently, bile acid–FXR regulation has been reported to play an integral role in both hepatic and intestinal inflammation, and in atherosclerosis. In this study, we found that FXR knockout mice had more disease severity in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Obeticholic acid (6α-ethyl-Chenodeoxycholic Acid, 6-ECDCA), a synthetic FXR agonist, is an orally available drug that is currently in clinical trials for the treatment of inflammatory diseases such 
as alcoholic hepatitis, nonalcoholic steatohepatitis, and primary biliary cirrhosis. 
Study the mechanism of chenodeoxycholic acid (CDCA) of asthma and anti-inflammatory. Methods: nitrate reductase method to analyze the effect of CDCA serum and rat tracheal NO content; using competitive protein binding assay to analyze the effect of CDCA in rat tracheal tissue cAMP content; ultraviolet spectrophotometry analysis of CDCA in mice trachea and lung tissue of PGE2. Results: CDCA can significantly reduce serum and tracheal tissue of rats NO content; significantly increase the rat tracheal tissue in cAMP levels; significantly reduce the mouse trachea and lung tissue of PGE2. Conclusion: asthma and anti-inflammatory mechanism of CDCA and its increase cAMP levels in 
tracheal tissue and reduce the body related to the content of NO and PGE2.