Abstract

Recently, non-electrolyzed HOCl water has gained the attention of researchers as a new disinfecting agent owing to its high sterilization power, easy accessibility, and safety. Non-electrolyzed HOCl water was developed through mixing at a specific ratio based on hypochlorite and mineral supplements, which revealed a high oxidizing power. In this study, we investigated the effects of non-electrolyzed HOCl water on Helicobacter pylori (H. pylori) infection in C57BL/6 mice over 10 weeks. Mice were divided into three groups: normal control (NC) group supplied with purified water (PW) without infection, PW + H. pylori group supplied with PW after H. pylori infection, and HOCl + H. pylori group supplied with HOCl after H. pylori infection. Our findings demonstrated that the HOCl + H. pylori group greatly inhibited WBC and its differential counts, including total white blood cell (WBC), neutrophils, lymphocytes, monocytes, and eosinophils, when compared to the PW + H. pylori group. Accordingly, the amount of reactive oxygen species and calcium activity significantly decreased in the HOCl + H. pylori group compared to the PW + H. pylori group in both serum and stomach lysates. In contrast, HOCl water treatment enhanced GPx activity compared to PW treatment after H. pylori infection in both serum and stomach lysates. Accordingly, the levels of granulocyte-macrophage colony-stimulating factor, IL-1β, and TNF-α cytokine levels were significantly decreased in the HOCl + H. pylori group compared to those in the PW + H. pylori group in the stomach lysate; however, there was no significant difference in serum. In addition, the expression levels of Bax, MMP-3, MMP-9, and TLR-4 were found to decrease after HOCl water treatment, whereas the expression level of Bcl-2 was found to be enhanced after HOCl water treatment in the stomach lysate. Taken together, our results suggest that drinking non-electrolyzed HOCl water has positive anti-oxidative, anti-inflammatory, and anti-apoptotic effects in H. pylori-infected mice through redox and immune regulation.

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