Remote ischemic postconditioning protects the brain from global cerebral ischemia/reperfusion injury by up-regulating endothelial nitric oxide synthase through the PI3K/Akt pathway

Peng, Bei; Guo, Qulian; He, Zhijing; Liu, Yang; Yuan, Yajing; Wang, Na; Zhou, Jun

doi:10.1016/j.brainres.2012.01.033

Cited by 91 publications

(55 citation statements)

References 50 publications

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“…1 A remarkably neuroprotective role for both remote IPostC and brain IPostC have been demonstrated by us and other groups. [2][3][4][5] Oxidative stress from reactive oxygen species has long been considered as a key deleterious factor in cerebral I/R injury, 6 and one of the mechanisms of IPostC against I/R injury is its antioxidative function. 7 The phosphoinositide 3-kinase/Akt signaling pathway is a classical neuroprotective pathway against I/R injury and is involved in the antioxidative effect of limb remote IPostC.…”

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confidence: 99%

Ischemic Postconditioning Relieves Cerebral Ischemia and Reperfusion Injury Through Activating T-LAK Cell–Originated Protein Kinase/Protein Kinase B Pathway in Rats

Zhao

Wang

Tao

et al. 2014

Stroke

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Background and Purpose-Ischemic postconditioning (IPostC) protects against ischemic brain injury. To date, no study has examined the role of T-LAK-cell-originated protein kinase (TOPK) in IPostC-afforded neuroprotection. We explored the molecular mechanism related with TOPK in antioxidant effect of IPostC against ischemia/reperfusion. Methods-Focal ischemia was induced in rats by transient middle cerebral artery occlusion. Reactive oxygen species production in the peri-infarct cortex was detected using dihydroethidium. Malondialdehyde, as a marker of lipid peroxidation, and 3-nitrotyrosine, as a marker of protein oxidation, were detected by ELISA. The expression or location of antioxidant proteins and signal molecules TOPK, phosphatase, and tensin homolog, and Akt was analyzed by Western blotting and immunofluorescence. Results-Our results revealed that IPostC relieved transient middle cerebral artery occlusion-induced oxidative damage by reducing reactive oxygen species, malondialdehyde, and 3-nitrotyrosine accumulation in the peri-infarct cortex and raised levels of antioxidants perioxiredoxin-1, peroxiredoxin-2, and thioredoxin-1. In addition, IPostC increased p-AKT and p-TOPK levels, which colocalized in neural cells. In vitro TOPK knockdown by small interfering RNA decreased the levels of antioxidants peroxiredoxin-1, thioredoxin, and manganese superoxide dismutase activity in PC12 cells. In vivo intracerebroventricular injection of TOPK small interfering RNA reversed IPostC-induced neuroprotection by increasing infarct volume and nitric oxide content and reducing manganese superoxide dismutase activity. Moreover, IPostC-evoked Akt activation was blocked by TOPK small interfering RNA in vivo, but the decreased phosphorylated phosphatase and tensin homolog level in ischemia/reperfusion was not influenced by IPostC or by TOPK small interfering RNA treatment. Conclusions-Our

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confidence: 99%

Ischemic Postconditioning Relieves Cerebral Ischemia and Reperfusion Injury Through Activating T-LAK Cell–Originated Protein Kinase/Protein Kinase B Pathway in Rats

Zhao

Wang

Tao

et al. 2014

Stroke

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“…In a rat model of cardiac arrest and resuscitation, RIPoC attenuated post-resuscitation myocardial and cerebral dysfunction and improved the duration of survival [29]. However, it strongly needs to examine whether RIPoC can protect neurons from neuronal death induced by transient global cerebral ischemia, because only two studies regarding RIPoC-mediated neuroprotection have been reported [29,41]. Furthermore, no investigation into RIPoCmediated neuroprotective effect has been reported in a gerbil model of transient cerebral ischemia.…”

Section: Discussionmentioning

confidence: 95%

“…In preclinical studies regarding ischemic stroke, some researchers reported that RIPoC via the femoral artery occlusion reduced infarct volume in animal models of transient and permanent focal cerebral ischemia [15,27,37,40] as well as neonatal hypoxia/ischemia [30]. On the other hand, recently, Peng et al [41] first demonstrated that RIPoC effectively attenuated delayed neuronal death in the hippocampal CA1 region after ischemia-reperfusion using a rat model of transient forebrain ischemia. In a rat model of cardiac arrest and resuscitation, RIPoC attenuated post-resuscitation myocardial and cerebral dysfunction and improved the duration of survival [29].…”

Section: Discussionmentioning

confidence: 97%

Failure in neuroprotection of remote limb ischemic postconditioning in the hippocampus of a gerbil model of transient cerebral ischemia

Lee

Tae

Chen

et al. 2015

Journal of the Neurological Sciences

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“…LY294002 group (LY, n = 8): rats were injected with 5 μL pCMV4 lentivirus plasmids (icv) 2 weeks before MCAO [22], and injection of the phosphoinositide 3-kinase inhibitor LY294002 (10 μL, 10 mM, in 3% DMSO, icv) 15 min before MCAO [23]. They were then subjected to MCAO for 2 h followed by 24 h of reperfusion.…”

Section: Methodsmentioning

confidence: 99%

Protective Effect of SGK1 in Rat Hippocampal Neurons Subjected to Ischemia Reperfusion

Zhang

Qian

2014

Cell Physiol Biochem

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Background/Aims: To investigate the protective effect of SGK1 (serum- and glucocorticoid-inducible protein kinase 1) in rat hippocampal neurons in vitro and in vivo following ischemia reperfusion (I/R). Methods: Isolated rat hippocampal neurons were subjected to 2 h of oxygen and glucose deprivation (OGD) then returned to normoxic conditions for 10, 30 or 60 min. Cell apoptosis and protein expression of SGK1 were analyzed. To examine SGK1 function, we overexpressed SGK1 in rat hippocampal neurons. Finally we examined the involvement of PI3K/Akt/GSK3β signaling by treating the cells (untransfected or transfected with expression vector encoding SGK1) with the PI3K inhibitor LY294002. Findings were confirmed in vivo in a rat model of middle cerebral artery occlusion. Results: I/R caused a time-dependent increase in apoptosis, both in vitro and in vivo. SGK1 protein levels decreased significantly under the same conditions. Overexpression of SGK1 reduced apoptosis following OGD or I/R compared to cells transfected with empty vector and subjected to the same treatment, or sham-operated animals. Addition of LY294002 revealed that the action of SGK1 in suppressing apoptosis was mediated by the PI3K/Akt/GSK3β pathway. Conclusion: SGK1 plays a protective role in ischemia reperfusion in rat hippocampal neurons, exerting its effects via the PI3K/Akt/GSK3β pathway.

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Remote ischemic postconditioning protects the brain from global cerebral ischemia/reperfusion injury by up-regulating endothelial nitric oxide synthase through the PI3K/Akt pathway

Cited by 91 publications

References 50 publications

Ischemic Postconditioning Relieves Cerebral Ischemia and Reperfusion Injury Through Activating T-LAK Cell–Originated Protein Kinase/Protein Kinase B Pathway in Rats

Ischemic Postconditioning Relieves Cerebral Ischemia and Reperfusion Injury Through Activating T-LAK Cell–Originated Protein Kinase/Protein Kinase B Pathway in Rats

Failure in neuroprotection of remote limb ischemic postconditioning in the hippocampus of a gerbil model of transient cerebral ischemia

Protective Effect of SGK1 in Rat Hippocampal Neurons Subjected to Ischemia Reperfusion

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