Table 1.

Known FXR responses in experimental models of inflammation (SHP—small heterodimer protein; IL—interleukin; PPARα-UGT—peroxisome proliferator-activated receptor (PPARα)-UDP-glucuronosyltransferases (UGTs); Veg—vascular endothelial growth factor; FGF—fibroblast growth factor, IFN—interferon; madcam—mucosal addresin cell adhesion molecule).

Experimental Conditions	Intervention + Observed Effects
DSS Colitis	FXR Activation: ↑ IL10, SHP, FGF15, ↓IL1β ↑PPARα-UGT: ↓ FXR activity +worse injury PPARα-UGT KO mice: ↑FXR activity, ↓Injury Treatment with FGF15 analogue: ↓ IL1β, IL6, TNFα No effect in FXR KO mice
Ischemia Reperfusion Injury	FXR Activation Blunts increase Lactate, LDH, IL6, IL1β, IFNγ, Limits autophagic influx
Cirrhotic Rats	FXR Activation ↓ IFNγ, TNFα, MadCam-1, IL17, IL10
O/G Deprivation	FXR Activation ↑cell viability, ↓NFκB, TNFα, IL6
CDCA treatment in CACO-2	FXR Activation ↑IL8 IL6, TNFα, VegF FXR Inhibition Blunts Increases in IL8, IL6
High Fat Diet in Fish	↓FXR activity leads to increase in pro-inflammatory signaling CDCA dietary supplementation ↓IL1β, TNFα, COX-2, IL6 ↑ IL10