In study,we aimed to determine the mechanisms underlying the gastroprotective effects of sodium copper chlorophyllin (SCC) against ethanol-induced gastric ulcer injury in mice.First,the gastroprotective effects of SCC against gastric ulcer induced by ethanol were assessed.Then,biochemical,histopathological,immunohistochemistry assays,and weste blot analysis were conducted to determine the possible mechanisms of action underlying the effects of SCC.Compared to the effects of omeprazole (OME) in a confirmed mouse model of ethanolinduced gastric ulcer injury,treatment with various doses of SCC resulted in up-regulation of Bcl-2 and down-regulation of the pro-apoptotic protein Bax.Significant decreases in the levels of the malondialdehyde (MDA),myeloperoxidase (MPO),and NO in the gastric tissues were observed.Furthermore,inflammatory cytokine analysis revealed that SCC treatment inhibited the expressions of TNF-α and IL-6,greatly reduced the phosphorylation level of IκB,and repressed the nuclear translocation of N F-κB p65,which demonstrated that SCC inhibited the activation of the NF-κB pathway.The present findings suggest that the protective effects of SCC may be beneficial as a potential preventive and therapeutic agent for gastric ulcer through the NF-κB pathway.Taken together,SCC administration significantly decreased the levels of MPO,NO,and MDA in gastric tissue and exerted a powerful anti-inflammatory activity as demonstrated by reduction in the secretions of proinflammatory mediators such as IL-6 and TNF-α in the serum of mice exposed to ethanol.