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  1. Fulltext Effects of ischemic preconditioning of different intraoperative ischemic times of vascularized bone graft rabbit models
    Halim AS, Wan Ahmad Kamal WS, Noor NM, Abdullah S
    Arch Plast Surg, 2013 Nov;40(6):687-96.
    PMID: 24286040 DOI: 10.5999/aps.2013.40.6.687
    Ischemic preconditioning has been shown to improve the outcomes of hypoxic tolerance of the heart, brain, lung, liver, jejunum, skin, and muscle tissues. However, to date, no report of ischemic preconditioning on vascularized bone grafts has been published.
    Matched MeSH terms: Ischemic Preconditioning
  2. Fulltext Zinc Supplementation and Ischemia Pre-conditioning in Renal Ischemia/Reperfusion Injury
    Mazaheri B, Emami F, Moslemi F, Talebi A, Nematbakhsh M
    Malays J Med Sci, 2019 Jul;26(4):39-46.
    PMID: 31496892 DOI: 10.21315/mjms2019.26.4.5
    Backgrounds: Renal ischemia/reperfusion (RIR) is a major cause of kidney dysfunction in clinic. The main objective of this study was to investigate the effect of pre-conditioning ischemia (IPC) and zinc (Zn) supplementation on renal RIR injury.

    Methods: A total of 63 unilateral nephrectomised male and female Wistar rats were divided into five groups. Group 1 (ShOPR): Rats as sham-operated group were subjected to surgical procedure without RIR. Group 2 (Isch): Rats underwent RIR (left kidney ischemia for 30 min followed by 48 h reperfusion). Group 3 (Zn+Isch): Rats were treated as group 2 but they received Zn sulphate (30 mg/kg) 1 h before induction of RIR. Group 4 (IPC+Isch): Rats were treated as group 2 but they underwent 1 min of ischemia followed by 3 min reperfusion as IPC, which was repeated for three times before induction of RIR. Group 5 (Zn+IPC+Isch): Rats were subjected to receive both Zn sulphate and IPC before induction of RIR. Urine samples were collected in the last 6 h of reperfusion, and finally biochemical and histological measurements were performed.

    Results: The serum level of creatinine (Cr), normalised kidney weight (KW) and kidney tissue damage score (KTDS) increased by RIR alone significantly (P < 0.05). These parameters were attenuated statistically by Zn supplementation (P < 0.05). However, IPC alone or co-treatment of Zn and IPC did not improve the biochemical and histological markers altered by RIR injury.

    Conclusion: Zn supplementation had a protective role against RIR while such protective effect was not observed by IPC alone or by co-treatment of Zn and IPC.

    Matched MeSH terms: Ischemic Preconditioning
  3. Fulltext DJ-1 protects against cell death following acute cardiac ischemia-reperfusion injury
    Dongworth RK, Mukherjee UA, Hall AR, Astin R, Ong SB, Yao Z, et al.
    Cell Death Dis, 2014 Feb 27;5:e1082.
    PMID: 24577080 DOI: 10.1038/cddis.2014.41
    Novel therapeutic targets are required to protect the heart against cell death from acute ischemia-reperfusion injury (IRI). Mutations in the DJ-1 (PARK7) gene in dopaminergic neurons induce mitochondrial dysfunction and a genetic form of Parkinson's disease. Genetic ablation of DJ-1 renders the brain more susceptible to cell death following ischemia-reperfusion in a model of stroke. Although DJ-1 is present in the heart, its role there is currently unclear. We sought to investigate whether mitochondrial DJ-1 may protect the heart against cell death from acute IRI by preventing mitochondrial dysfunction. Overexpression of DJ-1 in HL-1 cardiac cells conferred the following beneficial effects: reduced cell death following simulated IRI (30.4±4.7% with DJ-1 versus 52.9±4.7% in control; n=5, P<0.05); delayed mitochondrial permeability transition pore (MPTP) opening (a critical mediator of cell death) (260±33 s with DJ-1 versus 121±12 s in control; n=6, P<0.05); and induction of mitochondrial elongation (81.3±2.5% with DJ-1 versus 62.0±2.8% in control; n=6 cells, P<0.05). These beneficial effects of DJ-1 were absent in cells expressing the non-functional DJ-1(L166P) and DJ-1(Cys106A) mutants. Adult mice devoid of DJ-1 (KO) were found to be more susceptible to cell death from in vivo IRI with larger myocardial infarct sizes (50.9±3.5% DJ-1 KO versus 41.1±2.5% in DJ-1 WT; n≥7, P<0.05) and resistant to cardioprotection by ischemic preconditioning. DJ-1 KO hearts showed increased mitochondrial fragmentation on electron microscopy, although there were no differences in calcium-induced MPTP opening, mitochondrial respiratory function or myocardial ATP levels. We demonstrate that loss of DJ-1 protects the heart from acute IRI cell death by preventing mitochondrial dysfunction. We propose that DJ-1 may represent a novel therapeutic target for cardioprotection.
    Matched MeSH terms: Ischemic Preconditioning, Myocardial
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