Ischemic Postconditioning During Reperfusion Attenuates Intestinal Injury and Mucosal Cell Apoptosis by Inhibiting JAK/STAT Signaling Activation

Wen, Sijian; Li, Yang; Li, Cai; Xia, Zhi-Qiu; Liu, Weifeng; Zhang, Xuyu; Lei, Wanlong; Huang, Wenqi; Liu, Ke-Xuan

doi:10.1097/shk.0b013e3182662266

Cited by 57 publications

(35 citation statements)

References 34 publications

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“…Allopurinol has been reported to attenuate reperfusion injury in various organs 12 . Moreover, tubular cell apoptosis has been found to be a major factor involved in the mechanism of renal IR injury 13 . Therefore, therapeutic approaches aimed at suppressing inflammatory responses and tubular apoptosis have been recognized to represent effective measures that may act to prevent renal injury and offer better prognosis after an I/R insult 14 .…”

Section: Introductionmentioning

confidence: 99%

Allopurinol preconditioning attenuates renal ischemia/reperfusion injury by inhibiting HMGB1 expression in a rat model

et al. 2016

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PURPOSE:To investigate the potential effects of pretreatment with allopurinol on renal ischemia/reperfusion injury (IRI) in a rat model. METHODS:Twenty four rats were subjected to right kidney uninephrectomy were randomly distributed into the following three groups (n=8): Group A (sham-operated group); Group B (ischemic group) with 30 min of renal ischemia after surgery; and Group C (allopurinol + ischemia group) pretreated with allopurinol at 50 mg/kg for 14 days. At 72 h after renal reperfusion, the kidney was harvested to assess inflammation and apoptosis. RESULTS:Pretreatment with allopurinol significantly improved renal functional and histological grade scores following I/R injury (p<0.05). Compared with Group B, the expression levels of caspase-3 and Bax were markedly reduced in Group C, meanwhile, whereas expression of bcl-2 was clearly increased (p<0.05). A newly described marker of inflammation, High Mobility Group Box 1(HMGB1), showed reduced expression in Group C (p<0.05). CONCLUSION:Pretreatment with allopurinol had a protective effect on kidney ischemia/reperfusion injury, which might be related to the inhibition of HMGB1 expression.Key words: Inflammation. Ischemia. Reperfusion. Allopurinol. Apoptosis. Rats. Allopurinol preconditioning attenuates renal ischemia/reperfusion injury by inhibiting HMGB1 expression in a rat model

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Section: Introductionmentioning

confidence: 99%

Allopurinol preconditioning attenuates renal ischemia/reperfusion injury by inhibiting HMGB1 expression in a rat model

et al. 2016

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“…Rapamycin has previously been shown to attenuate I/R-induced injury in the gut, pancreas, and heart. 8,36,37 Human colonic epithelial HCT116 cells, which Figure 3 Microbial induction of NOD2 expression in IECs is necessary for protection against injury. A: Germ free (GF), WT mice were subjected to ileal ischemia for 1 hour, and followed by 3 hours of reperfusion.…”

Section: Rapamycin Rescues Autophagy-mediated Protection Inmentioning

confidence: 99%

The Microbiota Protects against Ischemia/Reperfusion-Induced Intestinal Injury through Nucleotide-Binding Oligomerization Domain-Containing Protein 2 (NOD2) Signaling

Perez‐Chanona¹,

Mühlbauer²,

Jobin³

2014

The American Journal of Pathology

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Nucleotide-binding oligomerization domain-containing protein 2 (NOD2), an intracellular pattern recognition receptor, induces autophagy on detection of muramyl dipeptide (MDP), a component of microbial cell walls. The role of bacteria and NOD2 signaling toward ischemia/reperfusion (I/R)-induced intestinal injury response is unknown. Herein, we report that I/R-induced intestinal injury in germ-free (GF) C57BL/6 wild-type (WT) mice is worse than in conventionally derived mice. More important, microbiota-mediated protection against I/R-induced intestinal injury is abrogated in conventionally derived Nod2(-/-) mice and GF Nod2(-/-) mice. Also, WT mice raised in specific pathogen-free (SPF) conditions fared better against I/R-induced injury than SPF Nod2(-/-) mice. Moreover, SPF WT mice i.p. administered 10 mg/kg MDP were protected against injury compared with mice administered the inactive enantiomer, l-MDP, an effect lost in Nod2(-/-) mice. However, MDP administration failed to protect GF mice from I/R-induced intestinal injury compared with control, a phenomenon correlating with undetectable Nod2 mRNA level in the epithelium of GF mice. More important, the autophagy-inducer rapamycin protected Nod2(-/-) mice against I/R-induced injury and increased the levels of LC3(+) puncta in injured tissue of Nod2(-/-) mice. These findings demonstrate that NOD2 protects against I/R and promotes wound healing, likely through the induction of the autophagy response.

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“…IL-6 is able to worsen myocardial hypertrophy via activating the JAK/STAT pathway (21). The JAK/STAT pathway mediates the reduction in synthesis of the surface-active materials of pulmonary epithelial cells caused by oxidative stress (22). Coronary heart disease is typically accompanied by mitochondrial damage, which worsens coronary heart disease (23).…”

Section: Discussionmentioning

confidence: 99%

The effect of hydroxy safflower yellow A on coronary heart disease through Bcl‑2/Bax and PPAR‑γ

Zhou

Wang

et al. 2017

Exp Ther Med

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Abstract. The aim of the present study was to investigate the effect of hydroxy safflower yellow A (HSYA) on coronary heart disease through assessing the expression of B-cell lymphoma 2 (Bcl-2)/Bcl-2-like protein 4 (Bax) and peroxisome proliferator-activated receptor (PPAR)-γ. Coronary heart disease was induced in male Bama miniature swines via thoracoscope to serve as an animal model. Coronary heart disease swine were lavaged with 20 or 40 mg/kg HSYA. The mRNA levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-10, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were detected using reverse transcription-quantitative polymerase chain reaction. The protein expression of Bcl-2, Bax, PPAR-γ, phosphorylation of Janus kinase (JAK)2 and phosphorylation of signal transducer and activator of transcription (STAT)3 were detected using western blot analysis. Treatment with HSYA significantly suppressed the mRNA levels of IL-1β (P<0.01), IL-6 (P<0.01), TNF-α (P<0.01), COX-2 (P<0.01) and iNOS (P<0.01), and significantly increased IL-10 mRNA level in the coronary heart disease model (P<0.01). Furthermore, HSYA treatment significantly decreased the Bcl-2/Bax ratio (P<0.01) in the coronary heart disease model group, and enhanced the phosphorylation of JAK2/STAT3 pathway (P<0.01). However, HSYA had no significant effect on the expression of PPAR-γ protein. The results of the present study suggest that HSYA is able to weaken coronary heart disease via inflammation, Bcl-2/Bax and the PPAR-γ signaling pathway.

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Ischemic Postconditioning During Reperfusion Attenuates Intestinal Injury and Mucosal Cell Apoptosis by Inhibiting JAK/STAT Signaling Activation

Cited by 57 publications

References 34 publications

Allopurinol preconditioning attenuates renal ischemia/reperfusion injury by inhibiting HMGB1 expression in a rat model

Allopurinol preconditioning attenuates renal ischemia/reperfusion injury by inhibiting HMGB1 expression in a rat model

The Microbiota Protects against Ischemia/Reperfusion-Induced Intestinal Injury through Nucleotide-Binding Oligomerization Domain-Containing Protein 2 (NOD2) Signaling

The effect of hydroxy safflower yellow A on coronary heart disease through Bcl‑2/Bax and PPAR‑γ

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