Clinical Translation of Cerebral Preconditioning

Xi, Guohua

doi:10.1007/s12975-010-0012-x

Cited by 3 publications

(1 citation statement)

References 16 publications

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“…Various types of preconditioning, for example ischemic preconditioning, anesthetic preconditioning and pharmacological preconditioning over the past decades have resulted in various promising therapeutic effects for the treatment of patients with acute brain injury (Dirnagl, et al, 2009, Xi, 2010). HBO-PC, as one of the most common and attractive preconditioning strategies has been demonstrated to be neuroprotective in several animal models of neurological diseases, such as focal and global cerebral ischemia (Ostrowski, et al, 2008, Soejima, et al, 2012), spinal cord ischemia (Nie, et al, 2006), traumatic and surgical brain injury (Hu, et al, 2008, Jadhav, et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Hyperbaric oxygen preconditioning attenuates hyperglycemia-enhanced hemorrhagic transformation by inhibiting matrix metalloproteinases in focal cerebral ischemia in rats

Soejima

Krafft

et al. 2013

Experimental Neurology

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Hyperglycemia dramatically aggravates brain infarct and hemorrhagic transformation (HT) after ischemic stroke. Oxidative stress and matrix metalloproteinases (MMPs) play an important role in the pathophysiology of HT. Hyperbaric oxygen preconditioning (HBO-PC) has been proved to decrease oxidative stress and be neuroprotective in experimental stroke models. The present study determined whether HBO-PC would ameliorate HT by a pre-ischemic increase of reactive oxygen species (ROS) generation, and a suppression of MMP-2 and MMP-9 in hyperglycemic middle cerebral artery occlusion (MCAO) rats. Rats were pretreated with HBO (100% O2, 2.5 atmospheres absolute) 1 h daily for 5 days before MCAO. Acute hyperglycemia was induced by an injection of 50% dextrose. Neurological deficits, infarction volume and hemorrhagic volume were assessed 24 h and 7 days after ischemia. ROS scavenger n-acetyl cysteine (NAC), hypoxia-inducible factor-1α (HIF-1α) inhibitor 2-methoxyestradiol (2ME2) and activator cobalt chloride (CoCl2), and MMPs inhibitor SB-3CT were administrated for mechanism study. The activity of MMP-2 and MMP-9, and the expression HIF-1α were measured. HBO-PC improved neurological deficits, and reduced hemorrhagic volume; the expression of HIF-1α was significantly decreased, and the activity of MMP-2 and MMP-9 was reduced by HBO-PC compared with vehicle group. Our results suggested that HBO-PC attenuated HT via decreasing HIF-1α and its downstream MMP-2 and MMP-9 in hyperglycemic MCAO rats.

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Section: Introductionmentioning

confidence: 99%

Hyperbaric oxygen preconditioning attenuates hyperglycemia-enhanced hemorrhagic transformation by inhibiting matrix metalloproteinases in focal cerebral ischemia in rats

Soejima

Krafft

et al. 2013

Experimental Neurology

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Critical Role of the Sphingolipid Pathway in Stroke: a Review of Current Utility and Potential Therapeutic Targets

Sun

Keep

Hua

et al. 2016

Transl. Stroke Res.

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Sphingolipids are a series of cell membrane derived lipids which act as signaling molecules and play a critical role in cell death and survival, proliferation, recognition and migration. Sphingosine 1 phosphate acts as a key signaling molecule and regulates lymphocyte trafficking, glial cell activation, vasoconstriction, endothelial barrier function and neuronal death pathways which plays a critical role in numerous neurological conditions. Stroke is a second leading cause of death all over the world and effective therapies are still in great demand, including ischemic stroke and hemorrhagic stroke as well as the post stroke repair. Significantly, sphingolipid activities change after stroke and correlate with stroke outcome, which has promoted efforts to testify whether sphingolipid pathway could be a novel therapeutic target in stroke. Sphingolipid metabolic pathway, the connection between the pathway and stroke, as well as therapeutic interventions to manipulate the pathway to reduce stroke-induced brain injury are discussed in this review.

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Recurrent Transient Ischemic Attack Induces Neural Cytoskeleton Modification and Gliosis in an Experimental Model

Wang

Chaudhari

Winters

et al. 2022

Transl. Stroke Res.

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Clinical Translation of Cerebral Preconditioning

Cited by 3 publications

References 16 publications

Hyperbaric oxygen preconditioning attenuates hyperglycemia-enhanced hemorrhagic transformation by inhibiting matrix metalloproteinases in focal cerebral ischemia in rats

Hyperbaric oxygen preconditioning attenuates hyperglycemia-enhanced hemorrhagic transformation by inhibiting matrix metalloproteinases in focal cerebral ischemia in rats

Critical Role of the Sphingolipid Pathway in Stroke: a Review of Current Utility and Potential Therapeutic Targets

Recurrent Transient Ischemic Attack Induces Neural Cytoskeleton Modification and Gliosis in an Experimental Model

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