Acta Med. 2021, 64: 153-157
Gene Expression of Antioxidant Enzymes in the Resected Intestine in Crohn’s Disease
Introduction: The inflammatory process in Crohn’s disease (CD) is closely associated with the formation of reactive oxygen species. Antioxidant enzymes can play an important role in the outcome of CD and may influence postoperative recurrence in these patients. The aim of our study was to evaluate gene expression of intracellular antioxidant enzymes in surgically resected intestinal specimens of patients with CD, both in macroscopically normal and in inflamed tissue. Methods: A total of 28 patients referred for elective bowel resection were enrolled in the study. Full-thickness small intestinal specimens were investigated. Gene expression of antioxidant enzymes – superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione reductase (GSR) – was evaluated both in macroscopically normal and inflamed samples. Results: There were significantly lower levels of SOD1 mRNA (p = 0.007) and GSR mRNA (p = 0.027) in inflamed tissue compared to macroscopically normal areas. No significant differences were found between affected and non-affected intestinal segments in mRNA for SOD2, SOD3 and GPX. Conclusions: Our pilot data clearly showed that the gene expression of major antioxidant enzymes is not a uniform mechanism in the pathogenesis of Crohn’s disease. Topically decreased gene expression of SOD1 and GSR might facilitate the segmental tissue injury caused by reactive oxygen species.
Keywords
Crohn’s disease, gene expression, intestine, antioxidant enzymes, superoxide dismutase, glutathione peroxidase, glutathione reductase.
Funding
This work was supported by the project PROGRES Q40-15 and Q40-01 from Charles University and by MH CZ – DRO (UHHK, 00179906). The study was supported by A long-term organization development plan 1011 – Clinical fields (Faculty of Military Health Sciences 2016–2020).
References
Copyright
This is an open-access article distributed under the terms of the Creative Commons Attribution License.