TNF and ulcer disease: Specifically: (1) They counteract oxidative damage in AGU by increasing superoxide dismutase (SOD) activity, reducing malondialdehyde (MDA) levels [6,7], or activating the Nrf2/HO-1 pathway to scavenge reactive oxygen species (ROS); (2) They alleviate inflammatory infiltration at ulcer sites by inhibiting the release of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) via the NF-κB/MAPK pathway [8]; (3) They repair the tight junctions of gastric mucosal epithelium and enhance barrier function by upregulating the expression of occludin and claudin-1 [9,10].