Protective Effect of Peroxiredoxin 6 in Ischemia/Reperfusion-Induced Damage of Small Intestine

Gordeeva, A. E.; Temnov, A. A.; Charnagalov, Alexej; Шарапов, М. Г.; Фесенко, Е. Е.; Новоселов, В. И.

doi:10.1007/s10620-015-3809-3

Cited by 34 publications

(14 citation statements)

References 54 publications

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“…Our investigation demonstrated that MCB and mesenteric vessels have a common mechanism of reaction to I/R injury, which consists of decreased endothelium-dependent relaxation. According to our assumption, it is related to oxidative stress developed upon I/R injury of the small intestine [Bhattacharyya et al, 2014;Gordeeva et al, 2015], resulting in decreased NO bioavailability for vascular tone regulation [Garden and Granger, 2000;Vollmar and Menger, 2011].…”

Section: Discussionmentioning

confidence: 93%

Vascular Pathology of Ischemia/Reperfusion Injury of Rat Small Intestine

Gordeeva

Шарапов²,

Tikhonova³

et al. 2017

Cells Tissues Organs

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Ischemia/reperfusion (I/R) injury of the small intestine caused by occlusion of the superior mesenteric artery affects the intestinal tissue as well as components of the blood circulatory system from the microvasculature to mesenteric vessels. The aim of this work was to study the correlation between the dynamics of destruction development in the intestinal tissue, microvasculature, and mesenteric vessels in I/R of the small intestine. The microvasculature was analyzed by whole-organ continuous monitoring of the intestinal mucosal blood perfusion by laser Doppler flowmetry during the entire I/R. Real-time RT-PCR was used to assess gene expression of NF-κB, caspase-3, Ki67, and TNF-α in blood vessels. At the start of reperfusion, the first targets to be disrupted are microvessels in the apical villi. Injury of the apical part of the microcirculatory bloodstream correlates with the reduction in intestinal mucosal blood perfusion, which occurred simultaneously with apical villous destruction. By the end of the reperfusion period, the low intestinal mucosal blood perfusion is mirrored by the destruction of the microvasculature and mucosal structures in the entire organ. The development of mesenteric vessel injury is characterized by a change in NO metabolism and damaged endothelial cells concomitant with an alteration in the expression of genes encoding NF-κB, caspase-3, and Ki67 by the end of the reperfusion period. In I/R injury, detrimental effects on the intestinal tissue, microvasculature, and mesenteric vessels develop and exhibit common mechanisms of function, which show strong correlations.

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Section: Discussionmentioning

confidence: 93%

Vascular Pathology of Ischemia/Reperfusion Injury of Rat Small Intestine

Gordeeva

Шарапов²,

Tikhonova³

et al. 2017

Cells Tissues Organs

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“…To test the therapeutic effect of exogenous Prx1 and Prx2 proteins, the solution of the corresponding recombinant protein was injected into the tail vein to a final concentration of 20 μg/g of bodyweight 15 min before the beginning of ischemia. Selection of the injection method and the concentrations of protein solutions was carried out according to previous studies [ 13 , 14 ].…”

Section: Methodsmentioning

confidence: 99%

“…It must be noted that some Prx representatives have been investigated previously in models of artificially induced oxidative stress: total irradiation, renal ischemia-reperfusion injury, small intestine, etc. [ 13 , 14 , 15 , 16 , 17 ]. It is the Prx family proteins that have shown high efficiency in oxidative stress neutralization, which is associated with the high antioxidant activity of these enzymes and a wide range of neutralizable hydroperoxides, both organic and inorganic in nature.…”

Section: Introductionmentioning

confidence: 99%

Comparative Study of Protective Action of Exogenous 2-Cys Peroxiredoxins (Prx1 and Prx2) Under Renal Ischemia-Reperfusion Injury

et al. 2020

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The pathogenesis of ischemia-reperfusion (I/R) injuries is based on oxidative stress caused by a sharp increase in the concentration of free radicals, reactive oxygen species (ROS) and secondary products of free radical oxidation of biological macromolecules during reperfusion. Application of exogenous antioxidants lowers the level of ROS in the affected tissues, suppresses or adjusts the course of oxidative stress, thereby substantially reducing the severity of I/R injury. We believe that the use of antioxidant enzymes may be the most promising line of effort since they possess higher efficiency than low molecular weight antioxidants. Among antioxidant enzymes, of great interest are peroxiredoxins (Prx1–6) which reduce a wide range of organic and inorganic peroxide substrates. In an animal model of bilateral I/R injury of kidneys (using histological, biochemical, and molecular biological methods) it was shown that intravenous administration of recombinant typical 2-Cys peroxiredoxins (Prx1 and Prx2) effectively reduces the severity of I/R damage, contributing to the normalization of the structural and functional state of the kidneys and an almost 2-fold increase in the survival of experimental animals. The use of recombinant Prx1 or Prx2 can be an efficient approach for the prevention and treatment of renal I/R injury.

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“…Meanwhile, there are many reasons to believe that antioxidant enzymes can be more effective in neutralising reactive oxygen species (ROS) than low-molecular-weight antioxidants. Previously, we have shown the therapeutic effects of a recombinant peroxiredoxin 6 (PRDX6) in various pathologies associated with inflammation and oxidative stress, such as intestinal hypoxia/reperfusion [ 16 ]. We believe that PRDX6 may be effective as an agent that suppresses the level of oxidative stress in diabetes mellitus.…”

Section: Introductionmentioning

confidence: 99%

Peroxiredoxin 6 Attenuates Alloxan-Induced Type 1 Diabetes Mellitus in Mice and Cytokine-Induced Cytotoxicity in RIN-m5F Beta Cells

Новоселова

Глушкова

Лунин

et al. 2020

Journal of Diabetes Research

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Type 1 diabetes is associated with the destruction of pancreatic beta cells, which is mediated via an autoimmune mechanism and consequent inflammatory processes. In this article, we describe a beneficial effect of peroxiredoxin 6 (PRDX6) in a type 1 diabetes mouse model. The main idea of this study was based on the well-known data that oxidative stress plays an important role in pathogenesis of diabetes and its associated complications. We hypothesised that PRDX6, which is well known for its various biological functions, including antioxidant activity, may provide an antidiabetic effect. It was shown that PRDX6 prevented hyperglycemia, lowered the mortality rate, restored the plasma cytokine profile, reversed the splenic cell apoptosis, and reduced the β cell destruction in Langerhans islets in mice with a severe form of alloxan-induced diabetes. In addition, PRDX6 protected rat insulinoma RIN-m5F β cells, cultured with TNF-α and IL-1β, against the cytokine-induced cytotoxicity and reduced the apoptotic cell death and production of ROS. Signal transduction studies showed that PRDX6 prevented the activation of NF-κB and c-Jun N-terminal kinase signaling cascades in RIN-m5F β cells cultured with cytokines. In conclusion, there is a prospect for therapeutic application of PRDX6 to delay or even prevent β cell apoptosis in type 1 diabetes.

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Protective Effect of Peroxiredoxin 6 in Ischemia/Reperfusion-Induced Damage of Small Intestine

Abstract: The application of exogenous Prx6 enables normalization of the antioxidant status of the small intestine and reduction of cell destruction upon I/R-induced organ damage.

Cited by 34 publications

References 54 publications

Vascular Pathology of Ischemia/Reperfusion Injury of Rat Small Intestine

Vascular Pathology of Ischemia/Reperfusion Injury of Rat Small Intestine

Comparative Study of Protective Action of Exogenous 2-Cys Peroxiredoxins (Prx1 and Prx2) Under Renal Ischemia-Reperfusion Injury

Peroxiredoxin 6 Attenuates Alloxan-Induced Type 1 Diabetes Mellitus in Mice and Cytokine-Induced Cytotoxicity in RIN-m5F Beta Cells

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