IBD sites are subjected to stimulated polarization of macrophages to M1 type due to damage to intestinal tissues, which continuously release pro-inflammatory factors [interleukin (IL)-6, IL-1β], tumor necrosis factor alpha (TNF-α), and excessive pro-inflammatory factors further aggravate intestinal mucosal damage, excessive oxidative stress, etc. [4], resulting in nonspecific inflammation, mucosal barrier breakdown, and excessive oxidative stress in disease sites [5]. This evidence concerns the gene TNF and inflammatory bowel disease.