A Rat Model of Studying Tissue-Type Plasminogen Activator Thrombolysis in Ischemic Stroke With Diabetes

Fan, Xiang; Qiu, Jianhua; Yu, Zhanyang; Dai, Haibin; Singhal, Aneesh B.; Lo, Eng H.; Wang, Xiaoying

doi:10.1161/strokeaha.111.635250

Cited by 62 publications

(63 citation statements)

References 18 publications

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“…Ischemic stroke results in long-term disability and is a leading cause of mortality in developed countries (1,2). Early reperfusion is the most effective therapy for acute brain ischemia.…”

Section: Introductionmentioning

confidence: 99%

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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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“…Ischemic stroke results in long-term disability and is a leading cause of mortality in developed countries (1,2). Early reperfusion is the most effective therapy for acute brain ischemia.…”

Section: Introductionmentioning

confidence: 99%

“…Brain edema, traditionally classified as vasogenic and cytotoxic edema, serves a critical role in cerebral I/R injury (1,2,7). Cytotoxic edema occurs due to increased water permeability of cell membranes, which is associated with the aquaporin family, a group of selective water transport membrane proteins (8,9).…”

Section: Introductionmentioning

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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“…It is reported that hyperglycemia combined with cerebral ischemia-reperfusion model induces and exacerbates oxidative stress and poor reperfusion in the microcirculation of brain. 36,37 We previously reported that a high colloidal dispersion stability and biocompatibility of RNP improved a blood circulation for extended period.…”

Section: Discussionmentioning

confidence: 99%

Neurovascular Unit Protection From Cerebral Ischemia–Reperfusion Injury by Radical-Containing Nanoparticles in Mice

Hosoo

Marushima

Nagasaki

et al. 2017

Stroke

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C erebral large vessel occlusion is a life-threatening disease and causes neurological disorders. In addition to early recanalization with intravenous tissue plasminogen alteplase injection, multiple randomized control trials have recently demonstrated the efficacy and safety of mechanical thrombectomy using a stent retriever.1-6 However, reactive oxygen species (ROS) generation increases during reperfusion, which impairs survival and aggravates neurological function because of secondary brain injury, including hemorrhage in the ischemic area and brain edema. The functional disability rate was 30% to 70% after mechanical thrombectomy, and symptomatic hemorrhagic complication rate was up to 10%. [1][2][3][4][5][6] Oxidative stress suppression after reperfusion is a potential therapeutic strategy and can improve survival and the functional prognosis. Nitroxide (NO) radicals are free radical scavengers with known neuroprotective functions against cerebral ischemia in rodent models.7-9 The 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPOL) is a stable Background and Purpose-Reperfusion therapy by mechanical thrombectomy is used to treat acute ischemic stroke.However, reactive oxygen species generation after reperfusion therapy causes cerebral ischemia-reperfusion injury, which aggravates cerebral infarction. There is limited evidence for clinical efficacy in stroke for antioxidants. Here, we developed a novel core-shell type nanoparticle containing 4-amino-4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (nitroxide radical-containing nanoparticles [RNPs]) and investigated its ability to scavenge reactive oxygen species and confer neuroprotection. Methods-C57BL/6J mice underwent transient middle cerebral artery occlusion and then received RNPs (9 mg/kg) through the common carotid artery. Infarction size, neurological scale, and blood-brain barrier damage were visualized by Evans blue extravasation 24 hours after reperfusion. RNP distribution was detected by rhodamine labeling. Blood-brain barrier damage, neuronal apoptosis, and oxidative neuronal cell damage were evaluated in ischemic brains. Multiple free radicalscavenging capacities were analyzed by an electron paramagnetic resonance-based method. Results-RNPs were detected in endothelial cells and around neuronal cells in the ischemic lesion. Infarction size, neurological scale, and Evans blue extravasation were significantly lower after RNP treatment. RNP treatment preserved the endothelium and endothelial tight junctions in the ischemic brain; neuronal apoptosis, O 2 − production, and gene oxidation were significantly suppressed. Reactive oxygen species scavenging capacities against OH, ROO, and O 2 − improved by RNP treatment. Conclusions-An intra-arterial RNP injection after cerebral ischemia-reperfusion injury reduced blood-brain barrier damage and infarction volume by improving multiple reactive oxygen species scavenging capacities. Therefore, RNPs can provide neurovascular unit protection. Visual Overview-An online visual overview is available for this a...

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“…Insulin resistance is commonly present in patients with T2DM, hypertensive patients, elderly and obese populations, and in patients suffering from other vascular diseases 101. In T1DM rats subject to stroke, treatment with tPA increased brain hemorrhage, BBB permeability, and failed to improve neurological functional outcome while increasing inflammatory responses 102, 103. Another study reported that hyperglycemia during tPA infusion after stroke in rats increased BBB permeability and intracerebral hemorrhage, which may be mediated by oxidative stress mechanisms such as increasing superoxide production by nicotinamide adenine dinucleotide phosphate oxidase 104.…”

Section: Mechanisms Of Ischemia/reperfusion Damage In Diabetic Strokementioning

confidence: 99%

Blood–Brain Barrier Disruption, Vascular Impairment, and Ischemia/Reperfusion Damage in Diabetic Stroke

Venkat

Chopp

Chen

2017

JAHA

114

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A Rat Model of Studying Tissue-Type Plasminogen Activator Thrombolysis in Ischemic Stroke With Diabetes

Cited by 62 publications

References 18 publications

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

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

Neurovascular Unit Protection From Cerebral Ischemia–Reperfusion Injury by Radical-Containing Nanoparticles in Mice

Blood–Brain Barrier Disruption, Vascular Impairment, and Ischemia/Reperfusion Damage in Diabetic Stroke

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