Ischemic preconditioning and remote ischemic preconditioning have protective effect against cold ischemia–reperfusion injury of rat small intestine

Saeki, Isamu; Matsuura, Toshiharu; Hayashida, Miyeko; Taguchi, Tomoaki

doi:10.1007/s00383-010-2810-3

Cited by 32 publications

(22 citation statements)

References 24 publications

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“…RIPC, which can be achieved by noninvasive transient occlusion of blood flow to a limb with a blood pressure cuff, has been proven to be a valuable technique to reduce I/R injury in several organs (1,2), and newer studies also suggest RIPC-mediated protective effects on the intestine (18,19).…”

Section: Discussionmentioning

confidence: 99%

“…As a consequence, inflammation, sepsis and multiorgan failure may develop, leading to life-threatening conditions (14)(15)(16)(17). Although, protective effects of ischemic conditioning have intensively been described for the setting of myocardial I/R injury, recent studies suggest that the intestine may also benefit from this technique, showing a reduction of I/R-induced tissue injury by ischemic preconditioning, ischemic postconditioning and RIPC (18,19). However, the factors responsible for the RIPC-mediated effects in the intestine as well as the cellular mechanisms are currently unknown.…”

Section: Introductionmentioning

confidence: 99%

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Serum from Patients Undergoing Remote Ischemic Preconditioning Protects Cultured Human Intestinal Cells from Hypoxia-Induced Damage: Involvement of Matrixmetalloproteinase-2 and -9

Zitta

Meybohm

Bein

et al. 2011

Mol Med

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Remote ischemic preconditioning (RIPC) can be induced by transient occlusion of blood flow to a limb with a blood pressure cuff and exerts multiorgan protection from ischemia/reperfusion injury. Ischemia/reperfusion injury in the intestinal tract leads to intestinal barrier dysfunction and can result in multiple organ failure. Here we used an intestinal cell line (CaCo-2) to evaluate the effects of RIPC-conditioned patient sera on hypoxia-induced cell damage in vitro and to identify serum factors that mediate RIPC effects. Patient sera (n = 10) derived before RIPC (T0), directly after RIPC (T1) and 1 h after RIPC (T2) were added to the culture medium at the onset of hypoxia until 48 h after hypoxia. Reverse transcription-polymerase chain reaction, lactate dehydrogenase (LDH) assays, caspase-3/7 assays, silver staining, gelatin zymography and Western blotting were performed. Hypoxia led to morphological signs of cell damage and increased the release of LDH in cultures containing sera T0 (P < 0.01) and T1 (P < 0.05), but not sera T2, which reduced the hypoxia-mediated LDH release compared with sera T0 (P < 0.05). Gelatin zymography revealed a significant reduction of activities of the matrixmetalloproteinase (MMP)-2 and MMP-9 in the protective sera T2 compared with the nonprotective sera T0 (MMP-2: P < 0.01; MMP-9: P < 0.05). Addition of human recombinant MMP-2 and MMP-9 to MMP-deficient culture media increased the sensitivity of CaCo-2 cells to hypoxia-induced cell damage (P < 0.05), but did not result in a reduced phosphorylation of prosurvival kinases p42/44 and protein kinase B (Akt) or increased activity of caspase-3/7. Our results suggest MMP-2 and MMP-9 as currently unknown humoral factors that may be involved in RIPC-mediated cytoprotection in the intestine.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Serum from Patients Undergoing Remote Ischemic Preconditioning Protects Cultured Human Intestinal Cells from Hypoxia-Induced Damage: Involvement of Matrixmetalloproteinase-2 and -9

Zitta

Meybohm

Bein

et al. 2011

Mol Med

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“…However, the comparison between two independent groups, ALO-ALO and Fk-Fk-IPC, significance was observed (p = 0.035) to the beneficial effect of IPC-R in terms of development score. The role of IPC in reducing ischemic injury has been widely documented in a range of tissues, including IR injury of the small intestine [11][12][13][14][15][16] . A recent study shows that Ischemic preconditioning increased the intestinal stem cell activities in the intestinal crypts in mice 17 .…”

Section: Resultsmentioning

confidence: 99%

Remote ischemic preconditioning and tacrolimus in the fetal small bowel transplant in mice

et al. 2016

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PURPOSE:To evaluate the effect of remote ischemic preconditioning (IPC-R) in the fetal small bowel transplantation model. METHODS:Two groups were constituted: The Isogenic transplant (ISO, C57BL/6 mice, n=24) and the allogenic transplant (ALO, BALB/c mice, n=24). In each group, the animals were distributed with and without IPC-R. It was obtained the following subgroups: Tx, IPC-R, Fk, IPC-Fk, in both strains. Intestinal grafts were stained with hematoxylin and eosin and immunohistochemically. RESULTS:The graft development evaluation in ISO group showed that IPC-R reduced the development compared with ISO-Tx and Fk: 9.0±0.6). The graft rejection was lower in groups treated with IPC-R (-18%), Fk (-68%) or both (-61%) compared with ALO-Tx. CONCLUSION:Remote ischemic preconditioning showed benefic effect even associate with Tacrolimus on the development and acute rejection of the fetal small bowel graft in the Isogenic and Allogenic transplants.

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“…Since initial observations that exposure of organs to brief periods of non-lethal ischemia provides protection from injury against a subsequent lethal ischemic event [17] , many studies have established the concept of ischemic preconditioning (IP) in multiple organs [18][19][20] and across various species, including humans [18,21,22] . Unlike many pathologies characterized by a period of ischemia, liver transplantation presents an ideal model for therapies such as ischemic preconditioning as liver is exposed to a defined, scheduled, and relatively controlled period of cold ischemia.…”

Section: Ischemic Preconditioningmentioning

confidence: 99%

Redox therapeutics in hepatic ischemia reperfusion injury

Patel

Lang

Smith

et al. 2014

WJH

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Ischemia-reperfusion plays a major role in the injury experienced by the liver during transplantation. �uch work has been done recently investigating the role of redox species in hepatic ischemia-reperfusion. As animal models are better characterized and developed, and more insights are gained into the pathophysiology of hepatic ischemia reperfusion injury in humans the questions into exactly how oxidants participate in this injury are becoming more refined. These questions include effects of cellular location, timing of injury, and ability of therapeutics to access this site are increasing our appreciation of the complexity of ischemia reperfusion and improving attempts to ameliorate its effects. In this review, we aim to discuss the various methods to alter redox chemistry during ischemia reperfusion injury and future prospects for preventing organ injury during hepatic ischemia reperfusion.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved. Key words: Ischemia; Reperfusion; Pre-conditioning; NitriteCore tip: Reactive oxygen and nitrogen species play a central role in the pathology of ischemia-reperfusion injury. In this review we discuss the efforts of many groups to trial therapeutics to ameliorate this damage in animal models of disease as well as clinical trials in humans. The failure of some trials has served to highlight the complexity of timing and compartmentalization of Ischemia Reperfusion injury. Finally, we discuss the emerging potential of replenishing nitric oxide by nitrite therapy and the uniquely broad therapeutic profile of nitrite.Patel RP, Lang JD, Smith AB, Crawford JH. Redo�� therapeuRedo�� therapeutics in hepatic ischemia reperfusion injury.

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Ischemic preconditioning and remote ischemic preconditioning have protective effect against cold ischemia–reperfusion injury of rat small intestine

Abstract: Both IPC and RIPC were found to ameliorate ischemia-reperfusion injury after rat SBT in the early phase. HO-1 may therefore play a protective role against cold IRI.

Cited by 32 publications

References 24 publications

Serum from Patients Undergoing Remote Ischemic Preconditioning Protects Cultured Human Intestinal Cells from Hypoxia-Induced Damage: Involvement of Matrixmetalloproteinase-2 and -9

Serum from Patients Undergoing Remote Ischemic Preconditioning Protects Cultured Human Intestinal Cells from Hypoxia-Induced Damage: Involvement of Matrixmetalloproteinase-2 and -9

Remote ischemic preconditioning and tacrolimus in the fetal small bowel transplant in mice

Redox therapeutics in hepatic ischemia reperfusion injury

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