The tested drugs also exerted an anti-inflammatory effect by inhibiting the IAA-mediated increase of the transcription factor NF-κB, the inflammatory surrogate TNF-α, and their upstream molecule GSK-3β in addition to the oxidative stress marker MDA; this offers another mechanism for their anti-colitic effect since inflammation plays a pivotal role in the pathomechanism of ulcerative colitis (Uddin et al., 2013; Kwiecien et al., 2014). This evidence concerns the gene NFKB1 and ulcerative colitis.