Zinc supplementation alleviates oxidative stress to inhibit chronic gastritis via the ROS/NF-κB pathway in a mouse model.

Zinc (Zn) is an important trace element; it is involved in the regulation and maintenance of many physiological functions in organisms and has anti-inflammatory and antioxidant properties. Chronic gastritis is closely associated with damage to the gastric mucosa, which is detrimental to the health of humans and animals. There are few studies on the effects of zinc on, for example, gastric mucosal damage, oxidative stress, inflammation and cell death in mice. Therefore, we established in vivo and in vitro models of inflammatory injury and investigated the effects of zinc supplementation in C57BL/6 mice and Ges-1 cells and examined the expression of factors associated with oxidative stress, inflammation and cell death. In this study, the results of in vivo and in vitro experiments showed that reactive oxygen species (ROS) levels increased after sodium salicylate exposure. Malondialdehyde levels increased, the activity of the antioxidant enzymes catalase and superoxide dismutase decreased, and the activity of glutathione decreased. The NF-κB signaling pathway was activated, the levels of proinflammatory factors (TNF-α, IL-1β, and IL-6) increased, and the expression of cell death-related factors (Bax, Bcl-2, Caspase3, Caspase7, Caspase9, RIP1, RIP3, and MLKL) increased. Zinc supplementation attenuated the level of oxidative stress and reduced the level of inflammation and cell death. Our study indicated that sodium salicylate induced the production of large amounts of reactive oxygen species and activated the NF-κB pathway, leading to inflammatory damage and cell death in the mouse stomach. Zinc supplementation modulated the ROS/NF-κB pathway, reduced the level of oxidative stress, and attenuated inflammation and cell death in the mouse stomach and Ges-1 cells.