Ischemic postconditioning during reperfusion attenuates oxidative stress and intestinal mucosal apoptosis induced by intestinal ischemia/reperfusion via aldose reductase

Wen, Sijian; Ling, Yihong; Li, Yang; Cai, Li; Liu, Jiaxin; Li, Yunsheng; Yao, Xi; Xia, Zhi-Qiu; Liu, Ke-Xuan

doi:10.1016/j.surg.2012.09.017

Cited by 33 publications

(26 citation statements)

References 45 publications

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“…Increasing data support a viewpoint that varying degrees of multiple organ apoptosis occur during the pathogenesis of intestinal I/R [9, 10, 40]. Horie et al [14] found that rats exposed to intestinal I/R caused an increase in apoptotic hepatocytes.…”

Section: Discussionmentioning

confidence: 92%

Modulating the p66shc Signaling Pathway with Protocatechuic Acid Protects the Intestine from Ischemia-Reperfusion Injury and Alleviates Secondary Liver Damage

Wang

Chen

et al. 2014

The Scientific World Journal

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Intestinal ischemia-reperfusion (I/R) injury is a serious clinical pathophysiological process that may result in acute local intestine and remote liver injury. Protocatechuic acid (PCA), which has been widely studied as a polyphenolic compound, induces expression of antioxidative genes that combat oxidative stress and cell apoptosis. In this study, we investigated the effect of PCA pretreatment for protecting intestinal I/R-induced local intestine and remote liver injury in mice. Intestinal I/R was established by superior mesenteric artery occlusion for 45 min followed by reperfusion for 90 min. After the reperfusion period, PCA pretreatment markedly alleviated intestine and liver injury induced by intestinal I/R as indicated by histological alterations, decreases in serological damage parameters and nuclear factor-kappa B and phospho-foxo3a protein expression levels, and increases in glutathione, glutathione peroxidase, manganese superoxide dismutase protein expression, and Bcl-xL protein expression in the intestine and liver. These parameters were accompanied by PCA-induced adaptor protein p66shc suppression. These results suggest that PCA has a significant protective effect in the intestine and liver following injury induced by intestinal I/R. The protective effect of PCA may be attributed to the suppression of p66shc and the regulation of p66shc-related antioxidative and antiapoptotic factors.

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Section: Discussionmentioning

confidence: 92%

Modulating the p66shc Signaling Pathway with Protocatechuic Acid Protects the Intestine from Ischemia-Reperfusion Injury and Alleviates Secondary Liver Damage

Wang

Chen

et al. 2014

The Scientific World Journal

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“…Hematoxylin‐eosin (H&E) stained sections (4 μm) were evaluated independently by two pathologists blind to the study groups according to the Chiu’s and Eckhoff’s scores for the intestine and liver, respectively. Briefly, Chiu’s score was used as previously described . Liver tissues were evaluated at 200× magnification by a point‐counting method for the severity of hepatic injury using an ordinal scale as follows: grade 0, minimal or no evidence of injury; grade 1, mild injury consisting of cytoplasmic vacuolation, and focal nuclear pyknosis; grade 2, moderate to severe injury with extensive nuclear pyknosis, cytoplasmic hypereosinophilia, loss of intercellular borders, and mild to moderate neutrophil infiltration; and grade 3, severe injury with disintegration of hepatic cords, hemorrhage, and severe neutrophil infiltration.…”

Section: Methodsmentioning

confidence: 99%

“…17 In particular, we previously reported that HMGB1 is the major DAMP released from necroptotic enterocytes during intestinal I/R to induce an inflammatory response and subsequent intestinal damage. 18 Recent advances have revealed the intimate interplay between SIRS or sepsis-induced organ failure and cell death or cell dysfunction resulting from necrosis/necroptosis, 19,20 apoptosis, 21,22 and autophagy. 23 Necroptosis is a newly defined lytic type of cell death and a form of regulated necrosis that is inherently associated with inflammation and distinguished from other forms of cell death by the associated activation of the receptor-interacting protein kinase 1 and 3 (RIP1/3) necrosome complex and phosphorylation of mixed lineage kinase domain-like (MLKL).…”

Section: Introductionmentioning

confidence: 99%

HMGB1‐associated necroptosis and Kupffer cells M1 polarization underlies remote liver injury induced by intestinal ischemia/reperfusion in rats

Wen

Ling

et al. 2020

FASEB j.

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Reperfusion of the ischemic intestine often leads to drive distant organ injury, especially injuries associated with hepatocellular dysfunction. The precise molecular mechanisms and effective multiple organ protection strategies remain to be developed. In the current study, significant remote liver dysfunction was found after 6 hours of reperfusion according to increased histopathological scores, serum lactate dehydrogenase (LDH), alanine aminotransferase (ALT)/aspartate aminotransferase (AST) levels, as well as enhanced bacterial translocation in a rat intestinal ischemia/reperfusion (I/R) injury model. Moreover, receptor‐interacting protein kinase 1/3 (RIP1/3) and phosphorylated‐MLKL expressions in tissue were greatly elevated, indicating that necroptosis occurred and resulted in acute remote liver function impairment. Inhibiting the necroptotic pathway attenuated HMGB1 cytoplasm translocation and tissue damage. Meanwhile, macrophage‐depletion study demonstrated that Kupffer cells (KCs) are responsible for liver damage. Blocking HMGB1 partially restored the liver function via suppressed hepatocyte necroptosis, tissue inflammation, hepatic KCs, and circulating macrophages M1 polarization. What’s more, HMGB1 neutralization further protects against intestinal I/R‐associated liver damage in microbiota‐depleted rats. Therefore, intestinal I/R is likely associated with acute liver damage due to hepatocyte necroptosis, and which could be ameliorated by Nec‐1 administration and HMGB1 inhibition with the neutralizing antibody and inhibitor. Necroptosis inhibition and HMGB1 neutralization/inhibition, may emerge as effective pharmacological therapies to minimize intestinal I/R‐induced acute remote organ dysfunction.

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“…Recently, studies have been published on prevention/alleviation the effect of IR injury by inhibiting compliment system activation [33], by applying antioxidants [34,35], and trace elements [36]. Another trend for attenuating effects of IR injury is ischemic postconditioning [37-39]. …”

Section: Discussionmentioning

confidence: 99%

Examining the safety of colon anastomosis on a rat model of ischemia-reperfusion injury

Czeiger¹,

Osyntsov

et al. 2013

World J Emerg Surg

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IntroductionIntestinal ischemia and reperfusion can impair anastomotic strength.The purpose of this study was to evaluate the safety of delayed colon anastomosis following remote ischemia-reperfusion (IR) injury.MethodsRats divided into two groups underwent bilateral groin incisions, however only the study group had femoral artery clamping to inflict IR injury. Twenty-four hours following this insult, the animals underwent laparotomy, incision of the transverse colon and reanastomosis. End points included anastomotic leakage, strength and histopathological features.ResultsAnastomotic leak among IR animals (22.2%) was not statistically different in comparison to the controls [10.5% (p = 0.40)]. Anastomotic mean burst pressures showed no statistically significant difference [150.6 ± 15.57 mmHg in the control group vs. 159.9 ± 9.88 mmHg in the IR group (p = 0.64)]. The acute inflammatory process in the IR group was similar to controls (p = 0.26), as was the chronic repair process (p = 0.88). There was no significant difference between the inflammation:repair ratios amongst the two groups (p = 0.67).ConclusionPrimary colon repair is safe when performed 24 hours following systemic IR injury.

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Ischemic postconditioning during reperfusion attenuates oxidative stress and intestinal mucosal apoptosis induced by intestinal ischemia/reperfusion via aldose reductase

Cited by 33 publications

References 45 publications

Modulating the p66shc Signaling Pathway with Protocatechuic Acid Protects the Intestine from Ischemia-Reperfusion Injury and Alleviates Secondary Liver Damage

Modulating the p66shc Signaling Pathway with Protocatechuic Acid Protects the Intestine from Ischemia-Reperfusion Injury and Alleviates Secondary Liver Damage

HMGB1‐associated necroptosis and Kupffer cells M1 polarization underlies remote liver injury induced by intestinal ischemia/reperfusion in rats

Examining the safety of colon anastomosis on a rat model of ischemia-reperfusion injury

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