Delayed remote ischemic postconditioning protects against transient cerebral ischemia/reperfusion as well as kainate-induced injury in rats

Burda, Rastislav; Danielisová, Viera; Gottlieb, Miroslav; Némethová, Miroslava; Bonova, Petra; Matiasova, Milina; Morochovič, Radoslav; Bürda, Jozef

doi:10.1016/j.acthis.2014.04.011

Cited by 15 publications

(13 citation statements)

References 27 publications

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“…Our results using the remote tolerance [18] led us to the idea to apply combination of two sublethal stresses, "preconditioning and postconditioning", was applied on donor animals. This led to the development of full strength tolerance in the blood of the donors.…”

Section: Introductionmentioning

confidence: 99%

The End Effector of Ischemic Tolerance Present in Blood Plasma from Double Conditioned Donors Ameliorates Trimethyltin Provoked Damage in Brain

Burda¹,

Danielisová²,

Bürda³

2019

obm neurobiol

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Background: Many experiments have been done to demonstrate robust ischemic tolerance efficiency using mostly young and healthy animals. However, the translation of these results to usually elderly and sick patients moreover taking many various medicines has to date been disappointing. 3-Methyltin (TMT) poisoning and short-term transient cerebral ischemia cause similar damage, especially, to selectively vulnerable brain regions such as hippocampal CA1 and CA3. Methods: Using dual conditioning, we activated the full ischemic tolerance the products of which are located to blood plas ma. As s ublethal stresses, two periods of 20-minute hind-limb ischemia was used with a two-day interval in rats. Active plas ma was isolated 6 h after the second hind limb ischemia. Brain damage was detected by visualizing dead neurons by Fluoro-Jade B s taining and neuronal s urvival by NeuN immunoreaction. The functional capabilities of the surviving neurons were monitored by the Morris water maze.

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Section: Introductionmentioning

confidence: 99%

The End Effector of Ischemic Tolerance Present in Blood Plasma from Double Conditioned Donors Ameliorates Trimethyltin Provoked Damage in Brain

Burda¹,

Danielisová²,

Bürda³

2019

obm neurobiol

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“…Limb remote ischemic post-conditioning (RIPostC) is a novel post-conditioning procedure which involves repeated occlusion/release cycles on bilateral limb arteries ( 4 ). Unlike classical pre- or post-ischemic conditioning, limb RIPostC is easily adaptable in clinical practice and particularly suitable for long term rehabilitation ( 5 – 7 ). Numerous studies have demonstrated that limb RIPostC improves neurological outcomes in ischemic animal models ( 5 , 8 ).…”

Section: Introductionmentioning

confidence: 99%

“…Unlike classical pre- or post-ischemic conditioning, limb RIPostC is easily adaptable in clinical practice and particularly suitable for long term rehabilitation ( 5 – 7 ). Numerous studies have demonstrated that limb RIPostC improves neurological outcomes in ischemic animal models ( 5 , 8 ). However, there are few studies regarding the effect on hemorrhagic stroke and the mechanisms behind RIPostC.…”

Section: Introductionmentioning

confidence: 99%

Limb remote ischemic post‑conditioning reduces injury and improves long‑term behavioral recovery in rats following subarachnoid hemorrhage: Possible involvement of the autophagic process

Yang

et al. 2017

Mol Med Report

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Hemorrhage-related neurologic injury is a primary cause of disability and mortality following subarachnoid hemorrhage (SAH). The aim of the present study was to investigate the potential neuroprotective effect and the possible role of autophagy in limb remote ischemic post-conditioning (RIPostC) using an endovascular puncture rat model of SAH. RIPostC was induced by three cycles of occlusion (10 min) and release (10 min) in the bilateral femoral artery using an aneurysm clip. Early RIPostC began immediately following SAH, delayed RIPostC began following a 30 min delay and the repeated RIPostC group underwent the protocol every day for 3 days. Brain water content, SAH grading, terminal deoxynucleotidyl transferase dUTP nick end labeling-DAPI staining, transmission electron microscopy, and neurological and behavioral tests were conducted three days following surgery. Long term outcomes of behavior and memory were assessed using a rotarod test and Morris water maze test 1 month subsequently. Biomarkers of autophagy, including Beclin-1 and light chain 3 (LC3), were assessed using western blotting. The results of the present study demonstrated that, compared with other groups, repeated RIPostC was able to alleviate brain edema, prevent neuronal apoptosis, and improve short term and long term neurological function and memory. Beclin-1 and LC3 in the cortex were upregulated following treatment with repeated RIPostC. Autolysosomes increased 3 days following SAH and were maintained for 1 month in the repeated RIPostC group. Therefore, the present study indicated that the optimized repeated RIPostC may provide a noninvasive strategy to induce neuroprotection, and improve the short and long term outcomes of SAH-related cerebral injury, possibly involving the autophagy pathway.

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“…In a study by Burda et al, postconditioning performed by occlusion of the internal carotid artery 48 hours after ischemia-reperfusion in a rat model of cerebral ischemia resulted in significant improvements in the structure and function of nerve cells [21]. However, other researchers have reported that remote ischemic postconditioning involving occlusion of arteries in the hind limb results in significant neuroprotective effects when the treatment is initiated at 3 and 6 hours after reperfusion [22].…”

Section: The Protective Parameters Of Ischemic Postconditioningmentioning

confidence: 99%

“…Ischemic postconditioning activates NMDA2A receptors, promotes the internal flow of calcium ions, influences the ERK pathway and the synthesis of NO, and restores hippocampal blood flow [58]. Ischemic postconditioning can also inhibit some types of NMDA receptors, such as kainate receptors, in order to reduce glutamine toxicity and promote the recovery of cognitive function [21]. Cerebral ischemic postconditioning also influences KCC2 pathways and regulates the expression of gamma-aminobutyric acid receptors, resulting in improvements in cognitive dysfunction following stroke [59].…”

Section: Neuroprotective Effects Of Ischemic Postconditioningmentioning

confidence: 99%

Overview of Experimental and Clinical Findings regarding the Neuroprotective Effects of Cerebral Ischemic Postconditioning

Feng

Deng

et al. 2017

BioMed Research International

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Research on attenuating the structural and functional deficits observed following ischemia-reperfusion has become increasingly focused on the therapeutic potential of ischemic postconditioning. In recent years, various methods and animal models of ischemic postconditioning have been utilized. The results of these numerous studies have indicated that the mechanisms underlying the neuroprotective effects of ischemic postconditioning may involve reductions in the generation of free radicals and inhibition of calcium overload, as well as the release of endogenous active substances, alterations in membrane channel function, and activation of protein kinases. Here we review the novel discovery, mechanism, key factors, and clinical application of ischemic postconditioning and discuss its implications for future research and problem of clinical practice.

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Delayed remote ischemic postconditioning protects against transient cerebral ischemia/reperfusion as well as kainate-induced injury in rats

Cited by 15 publications

References 27 publications

The End Effector of Ischemic Tolerance Present in Blood Plasma from Double Conditioned Donors Ameliorates Trimethyltin Provoked Damage in Brain

The End Effector of Ischemic Tolerance Present in Blood Plasma from Double Conditioned Donors Ameliorates Trimethyltin Provoked Damage in Brain

Limb remote ischemic post‑conditioning reduces injury and improves long‑term behavioral recovery in rats following subarachnoid hemorrhage: Possible involvement of the autophagic process

Overview of Experimental and Clinical Findings regarding the Neuroprotective Effects of Cerebral Ischemic Postconditioning

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