NFKB1 and arthritic joint disease: In a rat model of acute gout-like arthritis, SO strongly hindered the inflammatory reaction, thinning the inflammatory infiltrate, lowering the levels of inflammatory mediators (TNF-α, IL-1β, IL-6), impeding the activity of nuclear factor-κB (NF-κB) (at least in the mast cells) and complement system activation [97].