This study was designed to evaluate the gastroprotective effect of Kangfuxin (KFX), a Chinese patent medicine constituent isolated from American cockroach, on ethanol-induced gastric ulcer in mice and to elucidate the potential mechanisms of the effect involved. According to the results, mice treated with alcohol appeared obvious gastric mucosal injury, while treatment with Cimetidine (a positive control) and KFX significantly relieved the damage, along with decreased oxidative stress and apoptosis indexes. Subsequently, we conducted a label-free quantitative proteomic (LFQ) and found that NF-κB and PI3K/AKT signaling pathway participated in gastroprotective effect of KFX. Furthermore, Western blot analysis revealed that KFX treatment inhibited the expression of TNF-α, IL-1β, greatly reduced the phosphorylation level of IκB and repressed the nuclear translocation of NF-κB p65, which demonstrated that KFX inhibited the activation of NF-κB pathway. Meanwhile, the PI3K/AKT pathway was also involved in regulating the anti-inflammation effect. These findings define for the first time that the gastroprotective effects of KFX against gastric ulcer can be attributed to its role in NF-κB inhibition.
Keywords: Anti-apoptosis; Anti-inflammation; Gastric ulcer; KFX; PI3K/AKT/NF-κB; Proteomics.
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