NFKB1 and endothelial dysfunction: UDCA has been shown to inhibit endothelial dysfunction by mitigating endoplasmic reticulum stress [17], reducing the production of reactive oxygen species (ROS) [17–19], preventing the release of various pro-inflammatory cytokines, promoting the secretion of anti-inflammatory cytokines, and inhibiting the expression of nuclear factor κB (NF-κB) and inducible nitric oxide synthase (iNOS) induced by inflammation [19, 20].