The Effect of Exogenous Peroxiredoxin 6 on the State of Mesenteric Vessels and the Small Intestine in Ischemia–Reperfusion Injury

• Published in: Biophysics (Oxford) Vol. 62; no. 6; pp. 998 - 1008
• Main Authors: Sharapov, M. G., Gordeeva, A. E., Goncharov, R. G., Tikhonova, I. V., Ravin, V. K., Temnov, A. A., Fesenko, E. E., Novoselov, V. I.
• Format: Journal Article
• Language: English
• Published: Moscow Pleiades Publishing 01.11.2017; Springer Nature B.V
• Subjects: Antioxidants; Apoptosis; Biological and Medical Physics; Biophysics; Biophysics of Complex Systems; Cell death; Homeostasis; Intravenous administration; Ischemia; Microvasculature; Nitric-oxide synthase; Occlusion; Oxidative stress; Pathogenesis; Peroxiredoxin; Physics; Physics and Astronomy; Reperfusion; Rodents; Small intestine; intestine; peroxiredoxin 6; mesenteric vessels; ischemia–reperfusion; gene expression
• ISSN: 0006-3509; 1555-6654
• DOI: 10.1134/S0006350917060239

Oxidative stress is the main component of pathogenesis in ischemia–reperfusion injury. The administration of exogenous antioxidants suppresses oxidative stress and may decrease the severity of ischemia–reperfusion injury. The intestine is one of the most sensitive organs to the effect of ischemia–reperfusion. A rat model of a small intestine ischemia–reperfusion injury, based on occlusion of the superior mesenteric artery, was used in this work. Recombinant peroxiredoxin 6, a representative of an ancient family of peroxidases that are able to neutralize a broad range of both organic and inorganic peroxides, was used as an exogenous antioxidant. The intravenous administration of the exogenous peroxiredoxin 6 prior to ischemia–reperfusion minimizes tissue injury and reduces apoptotic cell death in the intestine and the mesenteric vessels. The impact of the exogenous peroxiredoxin 6 upon the NO level elevation in animal blood has been shown to be correlated with the enhanced inducible NO synthase expression. Thus, the use of exogenous peroxiredoxin 6 in ischemia–reperfusion injury of the intestine and the mesenteric vessels promotes normalization of the tissue redox homeostasis, structure protection, and restoration of the microvasculature.