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Journal articles on the topic 'Cerebral ischemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Zhao, Ling, Qiwei Liao, Yueting Zhang, Shufen Tan, Shuqing Li, and Tingyu Ke. "Ischemic Postconditioning Mitigates Retinopathy in Tree Shrews with Diabetic Cerebral Ischemia." Journal of Diabetes Research 2020 (February 12, 2020): 1–10. http://dx.doi.org/10.1155/2020/6286571.

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Ischemic postconditioning (PC) is proved to efficiently protect diabetic patients with acute myocardial infarction from ischemia-reperfusion injury. We aimed to explore the protective roles of ischemic PC on diabetic retinopathy in tree shrews with diabetic cerebral ischemia. A diabetic tree shrew model was established through high-fat diet feeding combined with streptozotocin (STZ) injection, while cortical thrombotic cerebral ischemia was induced photochemically. Tree shrews were divided into the normal control group, sham operation group, diabetes mellitus group, diabetes mellitus+cerebral

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2

Kanazawa, Masato, Tetsuya Takahashi, Masanori Ishikawa, Osamu Onodera, Takayoshi Shimohata, and Gregory J. del Zoppo. "Angiogenesis in the ischemic core: A potential treatment target?" Journal of Cerebral Blood Flow & Metabolism 39, no. 5 (2019): 753–69. http://dx.doi.org/10.1177/0271678x19834158.

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The ischemic penumbra is both a concept in understanding the evolution of cerebral tissue injury outcome of focal ischemia and a potential therapeutic target for ischemic stroke. In this review, we examine the evidence that angiogenesis can contribute to beneficial outcomes following focal ischemia in model systems. Several studies have shown that, following cerebral ischemia, endothelial proliferation and subsequent angiogenesis can be detected beginning four days after cerebral ischemia in the border of the ischemic core, or in the ischemic periphery, in rodent and non-human primate models,

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3

Wang, Lei, Xu Zhang, Xiaoxing Xiong, et al. "Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke." Antioxidants 11, no. 12 (2022): 2377. http://dx.doi.org/10.3390/antiox11122377.

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Cerebral ischemic stroke is characterized by acute ischemia in a certain part of the brain, which leads to brain cells necrosis, apoptosis, ferroptosis, pyroptosis, etc. At present, there are limited effective clinical treatments for cerebral ischemic stroke, and the recovery of cerebral blood circulation will lead to cerebral ischemia-reperfusion injury (CIRI). Cerebral ischemic stroke involves many pathological processes such as oxidative stress, inflammation, and mitochondrial dysfunction. Nuclear factor erythroid 2-related factor 2 (Nrf2), as one of the most critical antioxidant transcript

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4

Danilova, T. V. "Features of epilepsy in acute and chronic cerebral ischemia." Kazan medical journal 98, no. 6 (2017): 877–83. http://dx.doi.org/10.17750/kmj2017-877.

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Aim. To study clinical features, functional and neuroimaging characteristics of the brain of patients with ischemic brain disease and epileptic seizures. Methods. 772 patients with acute and chronic cerebral ischemia (265 stroke patients with epileptic seizures and 174 patients with seizures on the background of chronic cerebral ischemia, and 203 patients with stroke and 130 patients with chronic cerebral ischemia without seizures) were comprehensively examined. The clinical neurological examination, electroencephalography, magnetic resonance imaging, ultrasound duplex scanning of extra- and i

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Yamamoto, Kazumi, Fumiharu Akai, Toshiki Yoshimine, and Takehiko Yanagihara. "Immunohistochemical investigation of cerebral ischemia after middle cerebral artery occlusion in gerbils." Journal of Neurosurgery 67, no. 3 (1987): 414–20. http://dx.doi.org/10.3171/jns.1987.67.3.0414.

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✓ Progression and recovery of ischemic and postischemic damage after occlusion of the middle cerebral artery and subsequent reperfusion were investigated in the gerbil. This study was performed by immunohistochemical reaction testing for tubulin and creatine kinase BB-isoenzyme to visualize the neuronal structure and by immunohistochemical reaction testing for astroprotein (an astrocyte-specific protein) to visualize reactive astrocytes. The earliest ischemic lesion became visible in the frontoparietal cortex after 7 minutes of ischemia as a laminar loss of the reaction for tubulin involving t

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Duarte, Sinésio Grace, Antônio Dorival Campos, and Benedicto Oscar Colli. "Functional evaluation of temporary focal cerebral ischemia: experimental model." Arquivos de Neuro-Psiquiatria 61, no. 3B (2003): 751–56. http://dx.doi.org/10.1590/s0004-282x2003000500009.

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OBJECTIVE: Despite cerebral ischemia being a frequent clinical pathologic state, the tolerance of neural tissue to oxygen absence and to reperfusion is controversial. This study aims to evaluate the effects of focal cerebral ischemia/reperfusion, by analyzing the mitochondrial respiration. METHOD: Sixty-four adult rats underwent focal cerebral ischemia by middle cerebral artery occlusion, during 15, 30 and 60 minutes, followed by 10 minutes or 19 hours of reperfusion. The effects of ischemia were analyzed measuring the O2 consumption by mitochondria in the ischemic and non-ischemic areas. RESU

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7

Han, Xue Mei, Hong Tao Wei, and Song Yan Liu. "Involvement of Erythropoietin Expression in Acupuncture Preconditioning-Induced Ischemic Tolerance." Advanced Materials Research 554-556 (July 2012): 1650–55. http://dx.doi.org/10.4028/www.scientific.net/amr.554-556.1650.

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Abstract Objective To investigate the expression of erythropoietin (EPO) after acupuncture preconditioning plus focal cerebral ischemia treatment. Methods Rat focal cerebral ischemia model and acupuncture preconditioning model were established. Animals were randomly assigned into different groups: control (focal cerebral ischemia) and acupuncture preconditioning plus focal cerebral ischemia, with 8 rats for each group. The expression of EPO after different treatments was determined by histological examination, immunohistochemistry and in situ hybridization. Results The mRNA and protein express

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8

Dong, Chao, Jiawei Li, Ming Zhao, et al. "Pharmacological Effect of Panax notoginseng Saponins on Cerebral Ischemia in Animal Models." BioMed Research International 2022 (August 4, 2022): 1–12. http://dx.doi.org/10.1155/2022/4281483.

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Panax notoginseng saponins (PNS), bioactive compounds, are commonly used to treat ischemic heart and cerebral diseases in China and other Asian countries. Most previous studies of PNS have focused on the mechanisms underlying their treatment of ischemic cardiovascular diseases but not cerebral ischemic diseases. This study sought to explore the pharmacological mechanisms underlying the effectiveness of PNS in treating cerebral ischemic diseases. Different experimental cerebral ischemia models (including middle cerebral artery occlusion (MCAO) and the blockade of four arteries in rats, collagen

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9

Zeng, Xian-Si, Wen-Shuo Geng, Lei Chen, and Jin-Jing Jia. "Thioredoxin as a Therapeutic Target in Cerebral Ischemia." Current Pharmaceutical Design 24, no. 25 (2018): 2986–92. http://dx.doi.org/10.2174/1381612824666180820143853.

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Background: Cerebral ischemia is a common cause of disability and death. Ischemic brain injury results from complex pathological processes, including oxidative stress, inflammation, and apoptosis. Thioredoxin( Trx) is an important multifunctional protein, which regulates cellular redox status. Increasing studies have demonstrated that Trx provides a neuroprotective role against cerebral ischemia-induced injury. Methods: A systematic search of PMC and the PubMed Database was conducted to summarize the protective effects of Trx against cerebral ischemia. Results: This article reviews the underst

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Rehni, Ashish K., Pradeep Bhateja, and Nirmal Singh. "Diethyl dithiocarbamic acid, a possible nuclear factor kappa B inhibitor, attenuates ischemic postconditioning-induced attenuation of cerebral ischemia–reperfusion injury in mice." Canadian Journal of Physiology and Pharmacology 87, no. 1 (2009): 63–68. http://dx.doi.org/10.1139/y08-100.

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The present study was designed to pharmacologically investigate the possible role of nuclear factor kappa B (NF-κB) in the reversal of global cerebral injury induced by ischemia and reperfusion after ischemic postconditioning. Bilateral carotid artery occlusion for 17 min followed by reperfusion for 24 h was employed to produce ischemia- and reperfusion-induced cerebral injury in mice. Cerebral infarct size was measured by using triphenyltetrazolium chloride staining. Memory was evaluated using the Morris water maze test. The rotarod test was employed to assess motor incoordination. Bilateral

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11

Yagita, Yoshiki, Kazuo Kitagawa, Naoki Oyama, et al. "Functional Deterioration of Endothelial Nitric Oxide Synthase after Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 33, no. 10 (2013): 1532–39. http://dx.doi.org/10.1038/jcbfm.2013.112.

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Endothelial nitric oxide synthase (eNOS) dysfunction is related to secondary injury and lesion expansion after cerebral ischemia. To date, there are few reports about postischemic alterations in the eNOS regulatory system. The purpose of the present study was to clarify eNOS expression, Ser1177 phosphorylation, and monomer formation after cerebral ischemia. Male Wistar rats were subjected to transient focal cerebral ischemia. Endothelial nitric oxide synthase messenger RNA (mRNA) and protein expression increased ~ 8-fold in the ischemic lesion. In the middle cerebral artery core, eNOS-Ser1177

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Lee, Choong-Hyun, Tae-Kyeong Lee, Dae Won Kim, et al. "Relationship between Neuronal Damage/Death and Astrogliosis in the Cerebral Motor Cortex of Gerbil Models of Mild and Severe Ischemia and Reperfusion Injury." International Journal of Molecular Sciences 23, no. 9 (2022): 5096. http://dx.doi.org/10.3390/ijms23095096.

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Neuronal loss (death) occurs selectively in vulnerable brain regions after ischemic insults. Astrogliosis is accompanied by neuronal death. It can change the molecular expression and morphology of astrocytes following ischemic insults. However, little is known about cerebral ischemia and reperfusion injury that can variously lead to damage of astrocytes according to the degree of ischemic injury, which is related to neuronal damage/death. Thus, the purpose of this study was to examine the relationship between damage to cortical neurons and astrocytes using gerbil models of mild and severe tran

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13

Yu, Yong-Qiang, Lian-Cheng Liu, Fa-Cai Wang, et al. "Induction Profile of MANF/ARMET by Cerebral Ischemia and its Implication for Neuron Protection." Journal of Cerebral Blood Flow & Metabolism 30, no. 1 (2009): 79–91. http://dx.doi.org/10.1038/jcbfm.2009.181.

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Cerebral ischemia-induced accumulation of unfolded proteins in vulnerable neurons triggers endoplasmic reticulum (ER) stress. Arginine-rich, mutated in early stage tumors (ARMET) is an ER stress-inducible protein and upregulated in the early stage of cerebral ischemia. The purposes of this study were to investigate the characteristics and implications of ARMET expression induced by focal cerebral ischemia. Focal cerebral ischemia in rats was induced by right middle cerebral artery occlusion with a suture; ischemic lesions were assessed by magnetic resonance imaging and histology; neuronal apop

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Kitagawa, Kazuo, Masayasu Matsumoto, Takuma Mabuchi, et al. "Deficiency of Intercellular Adhesion Molecule 1 Attenuates Microcirculatory Disturbance and Infarction Size in Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 18, no. 12 (1998): 1336–45. http://dx.doi.org/10.1097/00004647-199812000-00008.

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Recent evidence has shown crucial roles for cell-adhesion molecules in inflammation-induced rolling, adhesion, and accumulation of neutrophils in tissue. Intercellular adhesion molecule-1 (ICAM-1) is one of these adhesion molecules. Previous studies have shown marked reduction in the size of infarction after focal cerebral ischemia by depletion of granulocytes and administration of the antibody against ICAM-1. In the present study we investigated the role of ICAM-1 in the size of ischemic lesions, accumulation of granulocytes, and microcirculatory compromise in focal cerebral ischemia by using

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15

Briones, Tess L., and Barbara Therrien. "Behavioral Effects of Transient Cerebral Ischemia." Biological Research For Nursing 1, no. 4 (2000): 276–86. http://dx.doi.org/10.1177/109980040000100404.

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CA1 neurons in the hippocampus, a brain structure involved in learning and memory, are selectively vulnerable to ischemic effects. In this study, the authors examined if duration of ischemia is directly related to extent of CA1 damage and degree of spatial learning deficit. Adult female Wistar rats received either 5-min or 10-min ischemia or sham surgery. Following recovery, rats were tested in the Morris water maze. Histological analysis showed moderate cell loss in CA1 (31%) and CA3 (12%) and minimal cell loss in CA2 (4%) with 5-min ischemia. Increased cell loss was seen in CA1 (68%), CA2 (1

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Liu, Zun-Jing, Wei Liu, Lei Liu, Cheng Xiao, Yu Wang, and Jing-Song Jiao. "Curcumin Protects Neuron against Cerebral Ischemia-Induced Inflammation through Improving PPAR-Gamma Function." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/470975.

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Cerebral ischemia is the most common cerebrovascular disease worldwide. Recent studies have demonstrated that curcumin had beneficial effect to attenuate cerebral ischemic injury. However, it is unclear how curcumin protects against cerebral ischemic injury. In the present study, using rat middle cerebral artery occlusion model, we found that curcumin was a potent PPARγagonist in that it upregulated PPARγexpression and PPARγ-PPRE binding activity. Administration of curcumin markedly decreased the infarct volume, improved neurological deficits, and reduced neuronal damage of rats. In addition,

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17

Song, Siying, Hao Wu, Xunming Ji, and Ran Meng. "The BE COOL Treatments (Batroxobin, oxygEn, Conditioning, and cOOLing): Emerging Adjunct Therapies for Ischemic Cerebrovascular Disease." Journal of Clinical Medicine 11, no. 20 (2022): 6193. http://dx.doi.org/10.3390/jcm11206193.

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Ischemic cerebrovascular disease (ICD), the most common neurological disease worldwide, can be classified based on the onset time (acute/chronic) and the type of cerebral blood vessel involved (artery or venous sinus). Classifications include acute ischemic stroke (AIS)/transient ischemic attack (TIA), chronic cerebral circulation insufficiency (CCCI), acute cerebral venous sinus thrombosis (CVST), and chronic cerebrospinal venous insufficiency (CCSVI). The pathogenesis of cerebral arterial ischemia may be correlated with cerebral venous ischemia through decreased cerebral perfusion. The core

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18

Chen, Chunli, Haiyun Qin, Jieqiong Tan, Zhiping Hu, and Liuwang Zeng. "The Role of Ubiquitin-Proteasome Pathway and Autophagy-Lysosome Pathway in Cerebral Ischemia." Oxidative Medicine and Cellular Longevity 2020 (February 1, 2020): 1–12. http://dx.doi.org/10.1155/2020/5457049.

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The ubiquitin-proteasome pathway and autophagy-lysosome pathway are two major routes for clearance of aberrant cellular components to maintain protein homeostasis and normal cellular functions. Accumulating evidence shows that these two pathways are impaired during cerebral ischemia, which contributes to ischemic-induced neuronal necrosis and apoptosis. This review aims to critically discuss current knowledge and controversies on these two pathways in response to cerebral ischemic stress. We also discuss molecular mechanisms underlying the impairments of these protein degradation pathways and

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Bon, Elizabeth, Nataliya Maksimovich, Sergei Zimatkin, Oksana Ostrovskaya, and Nikita Kokhan. "Comparative Characteristics of the Ultrastructure of the Pyramidal Neurons of the Parietal Cortex in Cerebral Ischemia of Varying Severity." Annals of Clinical Cytology and Pathology 9, no. 1 (2023): 1–6. http://dx.doi.org/10.47739/2475-9430.clinicalcytology.1147.

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Introduction: The ultra-structural characteristics of neuron organelles are important indicators of the degree of brain damage during ischemic exposure, which necessitates the study of changes in the ultrastructure of brain neurons. Methods: Models of subtotal, stepwise subtotal, partial and total cerebral ischemia were carried out on 24 outbred white male rats. Electron microscopy methods were used. Results: The data obtained indicate that with total cerebral ischemia the disturbances are more pronounced than with partial cerebral ischemia and stepwise subtotal cerebral ischemia. Conclusion:

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Peng, Cheng, Li-Ping Wang, Xia Tao, et al. "Preventive Cold Acclimation Augments the Reparative Function of Endothelial Progenitor Cells in Mice." Cellular Physiology and Biochemistry 45, no. 1 (2018): 175–91. http://dx.doi.org/10.1159/000486356.

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Background/Aims: Chronic cold exposure may increase energy expenditure and contribute to counteracting obesity, an important risk factor for cerebrocardiovascular diseases. This study sought to evaluate whether preventive cold acclimation before ischemia onset might be a promising option for preventing cerebral ischemic injury. Methods: After a 14-day cold acclimation period, young and aged mice were subjected to permanent cerebral ischemia, and histological analyses and behavioral tests were performed. Mouse endothelial progenitor cells (EPCs) were isolated, their function and number were det

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Alger, J. R., A. Brunetti, G. Nagashima, and K. A. Hossmann. "Assessment of Postischemic Cerebral Energy Metabolism in Cat by 31P NMR: The Cumulative Effects of Secondary Hypoxia and Ischemia." Journal of Cerebral Blood Flow & Metabolism 9, no. 4 (1989): 506–14. http://dx.doi.org/10.1038/jcbfm.1989.74.

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The sensitivity of cerebral energy metabolism to ischemic and hypoxic stresses following global cerebral ischemia was evaluated in a cat model using 31P nuclear magnetic resonance (NMR) spectroscopic methods. Complete global cerebral ischemia of 5 to 10 min in length was produced at 1 h intervals by reversible arterial occlusion, permitting continuous monitoring of NMR and EEG. Ischemia appeared to produce slightly more severe energy failure in animals that had previously experienced an ischemic injury. Preischemic hypoxia (5% O2 for 5 min) resulted in minor changes in the levels of phosphocre

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Ahad, Mohamad Anuar, Kesevan Rajah Kumaran, Tiang Ning, et al. "Insights into the neuropathology of cerebral ischemia and its mechanisms." Reviews in the Neurosciences 31, no. 5 (2020): 521–38. http://dx.doi.org/10.1515/revneuro-2019-0099.

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AbstractCerebral ischemia is a result of insufficient blood flow to the brain. It leads to limited supply of oxygen and other nutrients to meet metabolic demands. These phenomena lead to brain damage. There are two types of cerebral ischemia: focal and global ischemia. This condition has significant impact on patient’s health and health care system requirements. Animal models such as transient occlusion of the middle cerebral artery and permanent occlusion of extracranial vessels have been established to mimic the conditions of the respective type of cerebral ischemia and to further understand

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Kinuta, Yuji, Haruhiko Kikuchi, Masatsune Ishikawa, Mieko Kimura, and Yoshinori Itokawa. "Lipid peroxidation in focal cerebral ischemia." Journal of Neurosurgery 71, no. 3 (1989): 421–29. http://dx.doi.org/10.3171/jns.1989.71.3.0421.

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✓ To verify whether lipid peroxidation is associated with focal cerebral ischemia, a unilateral middle cerebral artery occlusion was carried out in rats. The concentrations of various endogenous antioxidants in the ischemic center were measured, including α-tocopherol and ubiquinones as lipid-soluble antioxidants and ascorbate as a water-soluble antioxidant. At 30 minutes after ischemia, α-tocopherol decreased to 79% of baseline, reduced ubiquinone-9 to 73%, ubiquinone-10 to 66%, and reduced ascorbate to 76%. Six hours after ischemia, α-tocopherol decreased to 63% and reached a plateau, wherea

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Lopez, Mary S., Robert J. Dempsey, and Raghu Vemuganti. "Resveratrol preconditioning induces cerebral ischemic tolerance but has minimal effect on cerebral microRNA profiles." Journal of Cerebral Blood Flow & Metabolism 36, no. 9 (2016): 1644–50. http://dx.doi.org/10.1177/0271678x16656202.

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The health benefits of the plant-derived polyphenol resveratrol were established in multiple disease systems. Notably, pre-treatment with resveratrol was shown to be neuroprotective in several models of cerebral ischemia. Mechanisms of resveratrol-mediated neuroprotection have been explored in the context of canonical resveratrol targets, but epigenetic and non-coding RNA processes have not yet been evaluated. Resveratrol was shown to alter microRNAs in cancer and cardiac ischemia. Previous studies also showed that ischemic preconditioning that induces ischemic tolerance significantly alters c

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Tranmer, Bruce I., Ted S. Keller, Glenn W. Kindt, and David Archer. "Loss of cerebral regulation during cardiac output variations in focal cerebral ischemia." Journal of Neurosurgery 77, no. 2 (1992): 253–59. http://dx.doi.org/10.3171/jns.1992.77.2.0253.

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✓ Focal cerebral ischemia was induced in anesthetized macaque monkeys by unilateral middle cerebral artery occlusion. The effect of blood volume expansion by a colloid agent and subsequent exsanguination to baseline cardiac output (CO) on local cerebral blood flow (CBF) was measured by the hydrogen clearance technique in both ischemic and nonischemic brain regions. Cardiac output was increased to maximum levels (159% ± 92%, mean ± standard error of the mean) by blood volume expansion with the colloid agent hetastarch, and was then reduced a similar amount (166% ± 82%) by exsanguination during

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Lin, Ming-Cheng, Chien-Chi Liu, Yu-Chen Lin, and Ching-Wen Hsu. "Epigallocatechin Gallate Modulates Essential Elements, Zn/Cu Ratio, Hazardous Metal, Lipid Peroxidation, and Antioxidant Activity in the Brain Cortex during Cerebral Ischemia." Antioxidants 11, no. 2 (2022): 396. http://dx.doi.org/10.3390/antiox11020396.

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Cerebral ischemia induces oxidative brain injury via increased oxidative stress. Epigallocatechin gallate (EGCG) exerts anti-oxidant, anti-inflammatory, and metal chelation effects through its active polyphenol constituent. This study investigates whether EGCG protection against cerebral ischemia-induced brain cortex injury occurs through modulating lipid peroxidation, antioxidant activity, the essential elements of selenium (Se), zinc (Zn), magnesium (Mg), copper (Cu), iron (Fe), and copper (Cu), Zn/Cu ratio, and the hazardous metal lead (Pb). Experimentally, assessment of the ligation group

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Shin, Tae Hwan, Da Yeon Lee, Shaherin Basith, et al. "Metabolome Changes in Cerebral Ischemia." Cells 9, no. 7 (2020): 1630. http://dx.doi.org/10.3390/cells9071630.

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Cerebral ischemia is caused by perturbations in blood flow to the brain that trigger sequential and complex metabolic and cellular pathologies. This leads to brain tissue damage, including neuronal cell death and cerebral infarction, manifesting clinically as ischemic stroke, which is the cause of considerable morbidity and mortality worldwide. To analyze the underlying biological mechanisms and identify potential biomarkers of ischemic stroke, various in vitro and in vivo experimental models have been established investigating different molecular aspects, such as genes, microRNAs, and protein

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Kim, Gyung W., Taku Sugawara, and Pak H. Chan. "Involvement of Oxidative Stress and Caspase-3 in Cortical Infarction after Photothrombotic Ischemia in Mice." Journal of Cerebral Blood Flow & Metabolism 20, no. 12 (2000): 1690–701. http://dx.doi.org/10.1097/00004647-200012000-00008.

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Apoptosis-related cell death is linked to oxidative stress and caspases in experimental cerebral ischemia, However, the role of oxidative stress in caspase activation and subsequent apoptotic cell death after cerebral ischemia is unknown, The authors evaluated the role of oxidative stress in ischemic cerebral infarction after photothrombosis and the relation between oxidative stress and caspase-related cell death 6 and 24 hours after ischemia with and without U-74389G, a potent free radical scavenger (10 mg/kg, 30 minutes before and after ischemia induction). Reactive oxygen species, detected

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Vongsfak, Jirapong, Wasana Pratchayasakul, Nattayaporn Apaijai, Tanat Vaniyapong, Nipon Chattipakorn, and Siriporn C. Chattipakorn. "The Alterations in Mitochondrial Dynamics Following Cerebral Ischemia/Reperfusion Injury." Antioxidants 10, no. 9 (2021): 1384. http://dx.doi.org/10.3390/antiox10091384.

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Cerebral ischemia results in a poor oxygen supply and cerebral infarction. Reperfusion to the ischemic area is the best therapeutic approach. Although reperfusion after ischemia has beneficial effects, it also causes ischemia/reperfusion (I/R) injury. Increases in oxidative stress, mitochondrial dysfunction, and cell death in the brain, resulting in brain infarction, have also been observed following cerebral I/R injury. Mitochondria are dynamic organelles, including mitochondrial fusion and fission. Both processes are essential for mitochondrial homeostasis and cell survival. Several studies

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Hong, Pu, Feng-Xian Li, Ruo-Nan Gu, et al. "Inhibition of NLRP3 Inflammasome Ameliorates Cerebral Ischemia-Reperfusion Injury in Diabetic Mice." Neural Plasticity 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/9163521.

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Sustained activation of NLRP3 inflammasome is closely related to diabetes and stroke. However, it is unknown whether NLRP3 inflammasome plays an essential role in stroke in diabetes. We aim to investigate the effect and the potential mechanism of NLRP3 inflammasome in diabetic mice with cerebral ischemia-reperfusion injury. A type 2 diabetic mouse model was induced by a high-fat diet and streptozotocin (STZ). Diabetic mice received MCC950 (the specific molecule NLRP3 inhibitor) or vehicle 60 minutes before the middle cerebral artery occlusion (MCAO) and reperfusion. MCC950 reduced the neurolog

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Hedayatpour, Azim, Maryam Shiasi, Peyman Modarresi, and Alieh Bashghareh. "Remote ischemic preconditioning combined with atorvastatin improves memory after global cerebral ischemia-reperfusion in male rats." Research Results in Pharmacology 8, no. 2 (2022): 27–35. http://dx.doi.org/10.3897/rrpharmacology.8.75753.

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Introduction: Damage to hippocampus can occur through ischemia. Memory problems are among the most significant disabilities after stroke. Therefore, improving memory is of great interest in helping post-stroke patients. This study demonstrated that intraperitoneally injection of atorvastatin with a short cycle of ischemia-reperfusion in the left femoral artery improved hippocampal CA1 neurons injury and memory problems after global cerebral ischemia. Materials and methods: In this article survey, we used 64 animals. Rats were divided into 8 groups, (n=8). Group 1: control; group 2: sham; gro

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Hedayatpour, Azim, Maryam Shiasi, Peyman Modarresi, and Alieh Bashghareh. "Remote ischemic preconditioning combined with atorvastatin improves memory after global cerebral ischemia-reperfusion in male rats." Research Results in Pharmacology 8, no. (2) (2022): 27–35. https://doi.org/10.3897/rrpharmacology.8.75753.

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Introduction: Damage to hippocampus can occur through ischemia. Memory problems are among the most significant disabilities after stroke. Therefore, improving memory is of great interest in helping post-stroke patients. This study demonstrated that intraperitoneally injection of atorvastatin with a short cycle of ischemia-reperfusion in the left femoral artery improved hippocampal CA1 neurons injury and memory problems after global cerebral ischemia. Materials and methods: In this article survey, we used 64 animals. Rats were divided into 8 groups, (n=8). Group 1: control; group 2: sham; group

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Li, Wangxiao, and Wei Zhang. "UTAC-Net: A Semantic Segmentation Model for Computer-Aided Diagnosis for Ischemic Region Based on Nuclear Medicine Cerebral Perfusion Imaging." Electronics 13, no. 8 (2024): 1466. http://dx.doi.org/10.3390/electronics13081466.

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Cerebral ischemia has a high morbidity and disability rate. Clinical diagnosis is mainly made by radiologists manually reviewing cerebral perfusion images to determine whether cerebral ischemia is present. The number of patients with cerebral ischemia has risen dramatically in recent years, which has brought a huge workload for radiologists. In order to improve the efficiency of diagnosis, we develop a neural network for segmenting cerebral ischemia regions in perfusion images. Combining deep learning with medical imaging technology, we propose a segmentation network, UTAC-Net, based on U-Net

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Marteau, Léna, Samuel Valable, Didier Divoux, et al. "Angiopoietin-2 is Vasoprotective in the Acute Phase of Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 33, no. 3 (2012): 389–95. http://dx.doi.org/10.1038/jcbfm.2012.178.

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Most forms of cerebral ischemia are characterized by damage to the entire neurovascular unit, which leads to an increase in the permeability of the blood–brain barrier (BBB). In response to permanent focal cerebral ischemia in mice, we detected an early concomitant increase in the expression of the vascular endothelial growth factor (VEGF), a key inducer of vascular leakage and pathological blood vessel growth, and of angiopoietin-2 (Ang2), which is closely associated with VEGF in vascular remodeling. Thus, the aim of this study was to evaluate the role of Ang2 alone, or in combination with VE

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Vechkanova, N., and N. Melnikova. "Study of ischemic depolarization in focal cerebral ischemia in rats." Genetics and breeding of animals, no. 2 (August 26, 2022): 70–75. http://dx.doi.org/10.31043/2410-2733-2022-2-70-75.

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Purpose: to study ischemic depolarization in focal cerebral ischemia in rats.Materials and methods. We conducted simulations of focal cerebral ischemia in 30 rats. The animals were divided into three groups: 1) normothermia (n = 10), 2) hypothermia (n = 10), 3) hyperthermia (n = 10). We identified a statistically significant correlation between the animal's body temperature and the number of episodes of depolarization. (r = 0,87, p<0,001). The average number of DC potential deviations in animals with hyperthermia was statistically significantly higher than in animals with normothermia. (p&l

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Juvela, Seppo, Matti Hillbom, and Markku Kaste. "Platelet thromboxane release and delayed cerebral ischemia in patients with subarachnoid hemorrhage." Journal of Neurosurgery 74, no. 3 (1991): 386–92. http://dx.doi.org/10.3171/jns.1991.74.3.0386.

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✓ Adenosine diphosphate-induced platelet aggregation and associated thromboxane B2 release were studied in 52 patients with subarachnoid hemorrhage (SAH) in order to detect a possible association between altered platelet function and development of cerebral ischemic complications after SAH. Compared to the values on admission, the patients showed significantly increased platelet aggregability (p < 0.05) and thromboxane release (p < 0.001) 1 to 2 weeks after SAH. The highest values of thromboxane release were seen in patients who deteriorated due to delayed cerebral ischemia with a perman

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Chen, Qun, Michael Chopp, Gordon Bodzin, and Hua Chen. "Temperature Modulation of Cerebral Depolarization during Focal Cerebral Ischemia in Rats: Correlation with Ischemic Injury." Journal of Cerebral Blood Flow & Metabolism 13, no. 3 (1993): 389–94. http://dx.doi.org/10.1038/jcbfm.1993.52.

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The role of cerebral depolarizations in focal cerebral ischemia is unknown. We therefore measured the direct current (DC) electrical activity in the cortex of Wistar rats subjected to transient occlusion of the middle cerebral artery (MCA). Focal ischemia was induced for 90 min by insertion of an intraluminal filament to occlude the MCA. To modulate cell damage, we subjected the rats to hypothermic (30°C, n = 4), normothermic (37°C, n = 4), and hyperthermic (40°C, n = 6) ischemia. Controlled temperatures were also maintained during 1 h of reperfusion. Continuous cortical DC potential changes w

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Fisher, Wink S. "Cerebral Ischemia." Neurosurgery 30, no. 5 (1992): 810. http://dx.doi.org/10.1097/00006123-199205000-00060.

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Westbrook, E. L. "Cerebral Ischemia." Neurology 42, no. 6 (1992): 1259. http://dx.doi.org/10.1212/wnl.42.6.1259.

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Hacke, Werner, Michael Hennerici, Herman J. Gelmers, Gunter Kramer, and Alan T. Marty. "Cerebral Ischemia." Critical Care Medicine 20, no. 6 (1992): 910. http://dx.doi.org/10.1097/00003246-199206000-00043.

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Wintzen, A. R. "Cerebral ischemia." Clinical Neurology and Neurosurgery 93, no. 4 (1991): 358. http://dx.doi.org/10.1016/0303-8467(91)90127-b.

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Wintzen, A. R. "Cerebral ischemia." Journal of the Neurological Sciences 67, no. 2 (1985): 265. http://dx.doi.org/10.1016/0022-510x(85)90124-8.

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Wintzen, A. R. "Cerebral ischemia." Journal of the Neurological Sciences 104, no. 1 (1991): 118. http://dx.doi.org/10.1016/0022-510x(91)90230-5.

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Fisher, Wink S. "Cerebral Ischemia." Neurosurgery 30, no. 5 (1992): 810. http://dx.doi.org/10.1227/00006123-199205000-00060.

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Bon, Lizaveta I., and Nataliya Y. Maksimovich. "Histological disorders of neurons of phylogenetically different parts of the cerebral cortex in partial, subtotal, stepwise subtotal, and total cerebral ischemia." Journal of Medical Science 90, no. 1 (2021): e493. http://dx.doi.org/10.20883/medical.e493.

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Aim. Measure of the histological changes in neurons in the parietal cortex and hippocampus of rats with partial, subtotal, stepwise subtotal, and total cerebral ischemia. Material and Methods. Studies were performed on 84 rats. Partial cerebral ischemia was modelled by ligation of one common carotid artery. Subtotal cerebral ischemia was modelled by ligation of both common carotid arteries. Stepwise subtotal cerebral ischemia was performed by sequential ligation of both common carotid artery with 7-day, 3-day or 1-day intervals. Total cerebral ischemia (CI) was modelled by decapitation. Result

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Rebel, Annette, John A. Ulatowski, Karena Joung, Enrico Bucci, Richard J. Traystman, and Raymond C. Koehler. "Regional cerebral blood flow in cats with cross-linked hemoglobin transfusion during focal cerebral ischemia." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 3 (2002): H832—H841. http://dx.doi.org/10.1152/ajpheart.00880.2001.

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841, 2002. First published November 8, 2001; 10.1152/ajpheart. 00880.2001.—The beneficial effect of hemodilution on cerebral blood flow (CBF) during focal cerebral ischemia is mitigated by reduced arterial oxygen content (CaO2 ). In anesthetized cats subjected to permanent middle cerebral artery occlusion, the time course of regional CBF was evaluated after isovolemic exchange transfusion with either albumin or a tetrameric hemoglobin-based oxygen carrier. The transfusion started 30 min after arterial occlusion. We tested the hypothesis that bulk oxygen transport (CBF × CaO2 ) to ischemic tiss

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Pettigrew, L. Creed, Mary L. Holtz, Susan D. Craddock, Stephen L. Minger, Nathan Hall, and James W. Geddes. "Microtubular Proteolysis in Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 16, no. 6 (1996): 1189–202. http://dx.doi.org/10.1097/00004647-199611000-00013.

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Calpain, a neutral protease activated by calcium, may promote microtubular proteolysis in ischemic brain. We tested this hypothesis in an animal model of focal cerebral ischemia without reperfusion. The earliest sign of tissue injury was observed after no more than 15 min of ischemia, with coiling of apical dendrites immunolabeled to show microtubule-associated protein 2 (MAP2). After 6 h of ischemia, MAP2 immunoreactivity was markedly diminished in the infarct zone. Quantitative Western analysis demonstrated that MAP2 was almost unmeasurable after 24 h of ischemia. An increase in calpain acti

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Wang, Yang, Yongting Wang, and Guo-Yuan Yang. "MicroRNAs in Cerebral Ischemia." Stroke Research and Treatment 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/276540.

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The risk of ischemic stroke increases substantially with age, making it the third leading cause of death and the leading cause of long-term disability in the world. Numerous studies demonstrated that genes, RNAs, and proteins are involved in the occurrence and development of stroke. Current studies found that microRNAs (miRNAs or miRs) are also closely related to the pathological process of stroke. miRNAs are a group of short, noncoding RNA molecules playing important role in posttranscriptional regulation of gene expression and they have emerged as regulators of ischemic preconditioning and i

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Zhang, Fangyi, Sherry Xu, and Costantino Iadecola. "Time Dependence of Effect of Nitric Oxide Synthase Inhibition on Cerebral Ischemic Damage." Journal of Cerebral Blood Flow & Metabolism 15, no. 4 (1995): 595–601. http://dx.doi.org/10.1038/jcbfm.1995.73.

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Nitric oxide, a potent vasodilator and an inhibitor of platelet aggregation, may be beneficial in the early stages of focal cerebral ischemia as it may facilitate collateral blood flow to the ischemic territory. Accordingly, the effect of inhibition of nitric oxide synthesis on cerebral ischemic damage may vary depending on the timing of the inhibition relative to the induction of ischemia. We therefore studied the time course of the effect of nitric oxide synthesis inhibition on focal cerebral ischemic damage. The middle cerebral artery was permanently occluded in spontaneously hypertensive r

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Yoshida, Mitsuyoshi, Kazuhiko Nakakimura, Ying Jun Cui, Mishiya Matsumoto, and Takefumi Sakabe. "Adenosine A1 Receptor Antagonist and Mitochondrial ATP-Sensitive Potassium Channel Blocker Attenuate the Tolerance to Focal Cerebral Ischemia in Rats." Journal of Cerebral Blood Flow & Metabolism 24, no. 7 (2004): 771–79. http://dx.doi.org/10.1097/01.wcb.0000122742.72175.1b.

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Involvement of adenosine and adenosine triphosphate-sensitive potassium (KATP) channels in the development of ischemic tolerance has been suggested in global ischemia, but has not been studied extensively in focal cerebral ischemia. This study evaluated modulating effects of adenosine A1 receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine) and mitochondrial KATP channel blocker 5HD (5-hydroxydecanoate) on the development of tolerance to focal cerebral ischemia in rats. Preconditioning with 30-minute middle cerebral artery occlusion (MCAO) reduced cortical and subcortical infarct volu

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