Renalase is localized to the small intestine crypt and expressed upon the activation of NF-κB p65 in mice model of fasting-induced oxidative stress

Aims: Renalase expression is regulated by Nuclear Factor (NF)-kappa B and hypoxia inducible factor (HIF)-1 alpha, and antioxidative stress function in renal cells were reported. However, dynamics of renalase and localizes in in-testine were remain unknown. We evaluated the effects of oxidative stress on renalase expression and locali-zation using model of fasting induced oxidative stress and Caco-2 cell, and examined the its physiological effects. Main methods: 24 male mice were divided into three groups: Control (Con), 72 h fasting (Fast), and 24 h refeeding after fasting (Refeed). Jejunum and ileum were collected respectively. The structure of jejunum and ileum were observed by hematoxylin and eosin (HE) stain. The expression levels of carbonylated protein, renalase, NF-kappa B p65 and HIF-1 alpha were measured by immunoblotting. Localization of renalase was observed by immunofluores-cent. in vitro assay was performed using Caco-2 cell. Renalase was overexpressed using adenovirus. After that, Caco-2 cell was treated with 2 mM H2O2 for 30 mM or 24 h. Key findings: Renalase was increased in Fast and it was localized in crypt. HIF-1 alpha did not increase, but NF-kappa B p65 increased in Fast. Renalase overexpression protects the Caco-2 cells against H2O2 induced oxidative stress. Significance: Renalase was localized in crypt and increased in Fast. This increase suggested protect response to oxidative stress because undifferenced cells were localized in crypt and need to be protected. Actually, renalase protected Caco-2 cells against H2O2 induced oxidative stress. Small intestinal renalase expression was regulated by NF-kappa B p65 and was considered to be a defense mechanism against oxidative stress.