Abstract
BackgroundThe aim of this study were to investigate whether selenium treatment attenuates lipid peroxidation and downregulates the NF-κB pathway in small intestinal mucosa and to examine whether the effect of selenium is also observed in oral buccal mucosa, during small intestinal IR injury.Materials and methodsEighteen rats were assigned into three groups: sham, IR, and IR + selenium. Saline or selenium was administered through a tail vein. 24 hours later, the superior mesenteric artery was exposed and clamped in the IR and IR + selenium groups. After ischemic and reperfusion period, animals were sacrificed and oral buccal mucosa and small intestinal mucosa were harvested.ResultsGlutathione peroxidase activity and cytoplasmic IκB-α expression was higher in the IR + selenium group than that in the IR group. A malondialdehyde level, cytoplasmic phosphorylated inhibitor κB-α, nuclear NF-κB p65 expressions, and NF-κB p65 DNA-binding activity were lower in the IR + selenium group than those in the IR group.ConclusionA selenium treatment may cause increased GPx activity, attenuated lipid peroxidation, and downregulated the NF-κB pathway during small intestinal IR injury. Furthermore, these therapeutic benefits of selenium can be observed in oral buccal mucosa as well as small intestinal mucosa.
Highlights
When the blood supply diminishes in metabolically active tissues, the tissue ischemia results in the so-called ischemic injury
A selenium treatment may cause increased Glutathione peroxidase (GPx) activity, attenuated lipid peroxidation, and downregulated the nuclear factor κB (NF-κB) pathway during small intestinal IR injury. These therapeutic benefits of selenium can be observed in oral buccal mucosa as well as small intestinal mucosa
Reduced glutathione (GSH) and Oxidized glutathione (GSSG) levels and GPx activity There were no significant differences in GSH and GSSG levels in oral buccal mucosa and small intestinal mucosa between the IR and IR + selenium groups
Summary
When the blood supply diminishes in metabolically active tissues, the tissue ischemia results in the so-called ischemic injury. When the blood flow restores, the reperfusion injury occurs. The development of reperfusion injury is mediated by reactive oxygen species (ROS) formation, lipid peroxidation, and inflammatory responses [2]. The small intestine is the most vulnerable organ to ischemia-reperfusion (IR) injury [3]. IR injury in the small intestine breaks mucosal barrier, which results in occurrence of systemic inflammatory response syndrome (SIRS). The mechanisms of the initiation and progression of SIRS during small intestinal IR injury are ROS formation, ROS-dependent inhibitor κB-α (IκB-α) phosphorylation in cytoplasm, and subsequent nuclear factor κB (NF-κB) activation in nucleus. The aim of this study were to investigate whether selenium treatment attenuates lipid peroxidation and downregulates the NF-κB pathway in small intestinal mucosa and to examine whether the effect of selenium is observed in oral buccal mucosa, during small intestinal IR injury
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