Transient Forebrain Ischemia Impact on Lymphocyte DNA Damage, Glutamic Acid Level, and SOD Activity in Blood

Kravčuková, Petra; Danielisová, Viera; Némethová, Miroslava; Bürda, Jozef; Gottlieb, Miroslav

doi:10.1007/s10571-009-9371-9

Cited by 23 publications

(23 citation statements)

References 51 publications

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“…Ischemia/reperfusion injury induces the release of neurotoxic amounts of glutamate and causes neuronal calcium overload, mtdNA leakage and mitochondrial membrane collapse (28,29). NAA, a surrogate marker of mitochondrial status, is a general marker of neuronal integrity viability (30) and a reservoir that maintains glutamate concentration at a safe level and prevents it from reaching excitotoxicity (31).…”

Section: Discussionmentioning

confidence: 99%

Exogenous carbon monoxide protects against mitochondrial DNA‑induced hippocampal pyroptosis in a model of hemorrhagic shock and resuscitation

Zhang

et al. 2020

Int J Mol Med

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carbon monoxide-releasing molecule-3 (cORM-3), which is an exogenous carbon monoxide (cO) compound, slowly releases cO under physiological conditions; this exerts neuroprotective effects against incomplete ischemia/reperfusion injury. The objective of the present study was to investigate whether the administration of cORM-3 protects against nucleotide-binding oligomerization domain-like receptor pyrin domain-3 (NLRP3) inflammasome formation and neuronal pyroptosis in the hippocampus following hemorrhagic shock and resuscitation (HSR). To establish this, an HSR model was created. Hemorrhagic shock was induced in adult male Sprague-Dawley rats under sevoflurane anesthesia by bleeding using a heparinized syringe to maintain a mean arterial pressure of 30±5 mmHg for 60 min. Resuscitation was performed by reperfusion of the blood and, if necessary, administering sterile saline to achieve the baseline arterial pressure. Following resuscitation, cORM-3 (4 mg/kg) was injected via the femoral vein. Neuronal pyroptosis in the hippocampus, mitochondrial morphology, mitochondrial dNA (mtdNA), brain magnetic resonance imaging, expression levels of NLRP3 and the interaction of pro-caspase-1 and apoptosis-associated speck-like protein containing a cARd domain (ASc) were examined 12 h after HSR; locomotor activity was assessed 7 days after HSR. compared with HSR-treated rats, cORM-3 administration resulted in a lower level of neuronal pyroptosis in the hippocampus, improved mitochondrial morphology, a lower mtdNA level, steadier levels of metabolites, decreased expression levels of NLRP3 and pro-caspase-1 interacting with ASc and enhanced locomotor activity. In conclusion, treatment with cORM-3 ameliorated impairments of locomotor and exploratory activities in a rat model of HSR. The mechanism may be associated with the inhibition of mitochondrial dNA-induced pyroptosis via improvements in cell metabolism.Abbreviations: cORM, carbon monoxide-releasing molecule; HSR, hemorrhage shock and resuscitation; NLRP3, nucleotide-binding oligomerization domain-like receptors pyrin domain-3; MRS, magnetic resonance spectroscopy

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Section: Discussionmentioning

confidence: 99%

Exogenous carbon monoxide protects against mitochondrial DNA‑induced hippocampal pyroptosis in a model of hemorrhagic shock and resuscitation

Zhang

et al. 2020

Int J Mol Med

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“…The production of superoxide was assessed by measuring the SOD-inhibited reduction of a water soluble tetrazolium salt (WST-1; Wuhan USCN Business Co., Ltd., Wuhan, China) as described previously (19,20). Briefly, xanthine-xanthine oxidase (Wuhan USCN Business Co., Ltd.) was used to generate a superoxide flux.…”

Section: Drug Treatmentmentioning

confidence: 99%

Resveratrol ameliorates oxidative stress and inhibits aquaporin 4 expression following rat cerebral ischemia-reperfusion injury

Tan

Liu

et al. 2015

Molecular Medicine Reports

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Abstract. Cerebral ischemia-reperfusion (I/R) is associated with increased levels of reactive oxygen species (ROS) and brain edema, which lead to the deterioration of patient prognosis. Resveratrol serves a neuroprotective role in I/R injury, and this role may be associated with its anti-oxidative effects. However, resveratrol's mechanism of action in cerebral I/R injury remains to be fully understood. In order to investigate the effect of resveratrol in cerebral I/R-induced injury, male Sprague-Dawley rats were randomly assigned to four groups: The sham-operation group, the I/R group and the edaravone and resveratrol groups (I/R + E and I/R + R groups). Infarct volume was evaluated by 2,3,5-tripenyltetrazolium chloride staining, brain edema was evaluated by the water content in the reperfused brain and malondialdehyde (MDA) was measured by the thiobarbituric acid method. Superoxide dismutase (SOD) levels were measured using the Total Superoxide Dismutase Assay kit. Inducible nitric oxide synthase (iNOS) levels in the hippocampus and cortex were measured by ELISA, and aquaporin 4 (AQP4) expression was measured by immunohistochemical staining and western blot analysis. The results demonstrated that resveratrol reduced the infarct volume and the incidence of brain edema and reduced neurological deficits. These outcomes were accompanied by reduced levels of MDA, iNOS and AQP4, and increased SOD levels in cerebral I/R injury. In conclusion, resveratrol protected against cerebral I/R injury by ameliorating oxidative stress and reducing AQP4 expression.

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“…Although the mechanism of delayed neuronal death has not been fully elucidated, some causes have been suggested. The delayed neuronal death is related to oxidative stress, intracellular calcium influx, glutamate receptor mediated neurotoxicity, and caspase-3 activation (Himi et al 1998;Won et al 2001;Rothstein et al 2002;Candelario-Jalil et al 2003;Al-Omar et al 2006;Kravcukova et al, 2009;Pavlíková et al, 2009;Racay et al, 2009). In addition, aging is one of the risk factors for stroke, and it is a primary factor in the development of greater ischemic neuronal damage in aged rats (Yao et al 1991;Saucier et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Comparison of Phosphorylated Extracellular Signal-Regulated Kinase 1/2 Immunoreactivity in the Hippocampal Ca1 Region Induced by Transient Cerebral Ischemia Between Adult and Aged Gerbils

et al. 2010

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In this study, the authors examined the difference of phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2) in the hippocampal CA1 region (CA1) between adult and aged gerbils after 5 min of transient cerebral ischemia. Delayed neuronal death in the CA1 of the aged group was much slower than that in the adult group after ischemia/reperfusion (I/R). pERK1/2 immunoreaction was observed in the CA1 region of the sham-operated adult gerbil. pERK1/2 immunoreactivity and protein levels in the ischemic CA1 region of the adult group were markedly increased 4 days after I/R, and then reduced up to 10 days after I/R. In contrast, pERK1/2 immunoreaction was hardly detected in the CA1 region of sham-operated aged gerbils, and the immunoreactivity increased from 1 day after the ischemic insult, and still observed until 10 days post-ischemia. In addition, pERK1/2-immunoreaction was expressed in astrocytes in the ischemic CA1 region: The expression in the ischemia-operated aged gerbils was later than that in the ischemia-operated adult gerbils. These results indicate that different patterns of ERK1/2 immunoreactivity may be associated with different processes of delayed neuronal death in adult and aged animals.

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Transient Forebrain Ischemia Impact on Lymphocyte DNA Damage, Glutamic Acid Level, and SOD Activity in Blood

Cited by 23 publications

References 51 publications

Exogenous carbon monoxide protects against mitochondrial DNA‑induced hippocampal pyroptosis in a model of hemorrhagic shock and resuscitation

Exogenous carbon monoxide protects against mitochondrial DNA‑induced hippocampal pyroptosis in a model of hemorrhagic shock and resuscitation

Resveratrol ameliorates oxidative stress and inhibits aquaporin 4 expression following rat cerebral ischemia-reperfusion injury

Comparison of Phosphorylated Extracellular Signal-Regulated Kinase 1/2 Immunoreactivity in the Hippocampal Ca1 Region Induced by Transient Cerebral Ischemia Between Adult and Aged Gerbils

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