Immediate postconditioning during reperfusion attenuates intestinal injury

Liu, Ke-Xuan; Li, Yunsheng; Huang, Wenqi; Chen, Shuqing; Wang, Zhongxin; Liu, Jiaxin; Xia, Zhengyuan

doi:10.1007/s00134-009-1428-1

Cited by 74 publications

(66 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…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%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

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.

show abstract

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

View full text Add to dashboard Cite

show abstract

“…However, IL-6 is a multifunctional cytokine with a variety of effects on cells and tissues. In intestine, IL-6 is induced in several injury models, including intestinal I/R injury and after surgical intestinal manipulation, and it promotes the inflammatory response (52,53). On the contrary, in vitro study has shown that IL-6 prevents death of rat intestinal epithelial cells subjected to hypoxia (54).…”

Section: Discussionmentioning

confidence: 99%

Treatment with Recombinant Trichinella spiralis Cathepsin B–like Protein Ameliorates Intestinal Ischemia/Reperfusion Injury in Mice by Promoting a Switch from M1 to M2 Macrophages

Liu

Wen

Zhan

et al. 2015

The Journal of Immunology

Self Cite

View full text Add to dashboard Cite

Intestinal ischemia/reperfusion (I/R) injury, in which macrophages play a key role, can cause high morbidity and mortality. The switch from classically (M1) to alternatively (M2) activated macrophages, which is dependent on the activation of STAT6 signaling, has been shown to protect organs from I/R injuries. In the current study, the effects of recombinant Trichinella spiralis cathepsin B–like protein (rTsCPB) on intestinal I/R injury and the potential mechanism related to macrophage phenotypes switch were investigated. In a mouse I/R model undergoing 60-min intestinal ischemia followed by 2-h or 7-d reperfusion, we demonstrated that intestinal I/R caused significant intestinal injury and induced a switch from M2 to M1 macrophages, evidenced by a decrease in levels of M2 markers (arginase-1 and found in inflammatory zone protein), an increase in levels of M1 markers (inducible NO synthase and CCR7), and a decrease in the ratio of M2/M1 macrophages. RTsCPB reversed intestinal I/R-induced M2–M1 transition and promoted M1-M2 phenotype switch evidenced by a significant decrease in M1 markers, an increase in M2 markers, and the ratio of M2/M1 macrophages. Meanwhile, rTsCPB significantly ameliorated intestinal injury and improved intestinal function and survival rate of animals, accompanied by a decrease in neutrophil infiltration and an increase in cell proliferation in the intestine. However, a selective STAT6 inhibitor, AS1517499, reversed the protective effects of rTsCPB by inhibiting M1 to M2 transition. These findings suggest that intestinal I/R injury causes a switch from M2 to M1 macrophages and that rTsCPB ameliorates intestinal injury by promoting STAT6-dependent M1 to M2 transition.

show abstract

“…Dear Sir: We thank Dr. Oltean and Olausson for their interest regarding our work [1]. We agree with Dr. Oltean and Olausson that the scoring system for intestinal ischemia-reperfusion initially proposed by Chiu [2] and later completed by Park et al [3] is reliable and reproducible.…”

mentioning

confidence: 60%

Reply to Oltean and Olausson

Liu

Huang

et al. 2010

Intensive Care Med

View full text Add to dashboard Cite

Immediate postconditioning during reperfusion attenuates intestinal injury

Abstract: Ischemic postconditioning reduces intestinal injury, in part, by inhibiting oxidative injury, neutrophils filtration and proinflammatory response. The early period of reperfusion is critical to intestinal protection by IPo, and intestinal protection with IPo can be enhanced by IPC.

Cited by 74 publications

References 33 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

Treatment with Recombinant Trichinella spiralis Cathepsin B–like Protein Ameliorates Intestinal Ischemia/Reperfusion Injury in Mice by Promoting a Switch from M1 to M2 Macrophages

Reply to Oltean and Olausson

Contact Info

Product

Resources

About