Artykuły w czasopismach na temat „Cerebral ischemia – Treatment”
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Kanazawa, Masato, Tetsuya Takahashi, Masanori Ishikawa, Osamu Onodera, Takayoshi Shimohata i Gregory J. del Zoppo. "Angiogenesis in the ischemic core: A potential treatment target?" Journal of Cerebral Blood Flow & Metabolism 39, nr 5 (6.03.2019): 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, although initial signals appear within hours of ischemia onset. Components of the neurovascular unit, its participation in new vessel formation, and the nature of the core and penumbra responses to experimental focal cerebral ischemia, are considered here. The potential co-localization of vascular remodeling and axonal outgrowth following focal cerebral ischemia based on the definition of tissue remodeling and the processes that follow ischemic stroke are also considered. The region of angiogenesis in the ischemic core and its surrounding tissue (ischemic periphery) may be a novel target for treatment. We summarize issues that are relevant to model studies of focal cerebral ischemia looking ahead to potential treatments.
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Siesjö, Bo K. "Pathophysiology and treatment of focal cerebral ischemia". Journal of Neurosurgery 77, nr 3 (wrzesień 1992): 337–54. http://dx.doi.org/10.3171/jns.1992.77.3.0337.
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✓ The mechanisms that give rise to ischemic brain damage have not been definitively determined, but considerable evidence exists that three major factors are involved: increases in the intercellular cytosolic calcium concentration (Ca++i), acidosis, and production of free radicals. A nonphysiological rise in Ca++i due to a disturbed pump/leak relationship for calcium is believed to cause cell damage by overactivation of lipases and proteases and possibly also of endonucleases, and by alterations of protein phosphorylation, which secondarily affects protein synthesis and genome expression. The severity of this disturbance depends on the density of ischemia. In complete or near-complete ischemia of the cardiac arrest type, pump activity has ceased and the calcium leak is enhanced by the massive release of excitatory amino acids. As a result, multiple calcium channels are opened. This is probably the scenario in the focus of an ischemic lesion due to middle cerebral artery occlusion. Such ischemic tissues can be salvaged only by recirculation, and any brain damage incurred is delayed, suggesting that the calcium transient gives rise to sustained changes in membrane function and metabolism. If the ischemia is less dense, as in the penumbral zone of a focal ischemic lesion, pump failure may be moderate and the leak may be only slightly or intermittently enhanced. These differences in the pump/leak relationship for calcium explain why calcium and glutamate antagonists may lack effect on the cardiac arrest type of ischemia, while decreasing infarct size in focal ischemia. The adverse effects of acidosis may be exerted by several mechanisms. When the ischemia is sustained, acidosis may promote edema formation by inducing Na+ and Cl− accumulation via coupled Na+/H+ and Cl−/HCO3− exchange; however, it may also prevent recovery of mitochondrial metabolism and resumption of H+ extrusion. If the ischemia is transient, pronounced intraischemic acidosis triggers delayed damage characterized by gross edema and seizures. Possibly, this is a result of free-radical formation. If the ischemia is moderate, as in the penumbral zone of a focal ischemic lesion, the effect of acidosis is controversial. In fact, enhanced glucolysis may then be beneficial. Although free radicals have long been assumed to be mediators of ischemic cell death, it is only recently that more substantial evidence of their participation has been produced. It now seems likely that one major target of free radicals is the microvasculature, and that free radicals and other mediators of inflammatory reactions (such as platelet-activating factor) aggravate the ischemic lesion by causing microvascular dysfunction and blood-brain barrier disruption. Solid experimental evidence exists that the infarct resulting from middle cerebral artery occlusion can be reduced by glutamate antagonists, by several calcium antagonists, and by some drugs acting on Ca++ and Na+ influx. In addition, published reports hint that qualitatively similar results are obtained with drugs whose sole or main effect is to scavenge free radicals. Thus, there is substantial experimental evidence that the ischemic lesions due to middle cerebral artery occlusion can be ameliorated by drugs, sometimes dramatically; however, the therapeutic window seems small, maximally 3 to 6 hours. This suggests that if these therapeutic principles are to be successfully applied to the clinical situation, patient management must change.
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Wang, Lei, Xu Zhang, Xiaoxing Xiong, Hua Zhu, Ran Chen, Shudi Zhang, Gang Chen i Zhihong Jian. "Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke". Antioxidants 11, nr 12 (30.11.2022): 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 transcription factors in cells, can coordinate various cytoprotective factors to inhibit oxidative stress. Targeting Nrf2 is considered as a potential strategy to prevent and treat cerebral ischemia injury. During cerebral ischemia, Nrf2 participates in signaling pathways such as Keap1, PI3K/AKT, MAPK, NF-κB, and HO-1, and then alleviates cerebral ischemia injury or CIRI by inhibiting oxidative stress, anti-inflammation, maintaining mitochondrial homeostasis, protecting the blood–brain barrier, and inhibiting ferroptosis. In this review, we have discussed the structure of Nrf2, the mechanisms of Nrf2 in cerebral ischemic stroke, the related research on the treatment of cerebral ischemia through the Nrf2 signaling pathway in recent years, and expounded the important role and future potential of the Nrf2 pathway in cerebral ischemic stroke.
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Siesjö, Bo K. "Pathophysiology and treatment of focal cerebral ischemia". Journal of Neurosurgery 108, nr 3 (marzec 2008): 616–31. http://dx.doi.org/10.3171/jns/2008/108/3/0616.
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✓ This article examines the pathophysiology of lesions caused by focal cerebral ischemia. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the focus are usually doomed unless reperfusion is quickly instituted. In contrast, although the penumbra contains cells “at risk,” these may remain viable for at least 4 to 8 hours. Cells in the penumbra may be salvaged by reperfusion or by drugs that prevent an extension of the infarction into the penumbral zone. Factors responsible for such an extension probably include acidosis, edema, K+/Ca++ transients, and inhibition of protein synthesis. Central to any discussion of the pathophysiology of ischemic lesions is energy depletion. This is because failure to maintain cellular adenosine triphosphate (ATP) levels leads to degradation of macromolecules of key importance to membrane and cytoskeletal integrity, to loss of ion homeostasis, involving cellular accumulation of Ca++, Na+, and Cl−, with osmotically obligated water, and to production of metabolic acids with a resulting decrease in intra- and extracellular pH. In all probability, loss of cellular calcium homeostasis plays an important role in the pathogenesis of ischemic cell damage. The resulting rise in the free cytosolic intracellular calcium concentration (Ca++) depends on both the loss of calcium pump function (due to ATP depletion), and the rise in membrane permeability to calcium. In ischemia, calcium influx occurs via multiple pathways. Some of the most important routes depend on activation of receptors by glutamate and associated excitatory amino acids released from depolarized presynaptic endings. However, ischemia also interferes with the intracellular sequestration and binding of calcium, thereby contributing to the rise in intracellular Ca++. A second key event in the ischemic tissue is activation of anaerobic glucolysis. The main reason for this activation is inhibition of mitochondrial metabolism by lack of oxygen; however, other factors probably contribute. For example, there is a complex interplay between loss of cellular calcium homeostasis and acidosis. On the one hand, a rise in intracellular Ca++ is apt to cause mitochondrial accumulation of calcium. This must interfere with ATP production and enhance anaerobic glucolysis. On the other hand, acidosis must interfere with calcium binding, thereby contributing to the rise in intracellular Ca++.
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Siesjö, Bo K. "Pathophysiology and treatment of focal cerebral ischemia". Journal of Neurosurgery 77, nr 2 (sierpień 1992): 169–84. http://dx.doi.org/10.3171/jns.1992.77.2.0169.
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✓ This article examines the pathophysiology of lesions caused by focal cerebral ischemia. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the focus are usually doomed unless reperfusion is quickly instituted. In contrast, although the penumbra contains cells “at risk.” these may remain viable for at least 4 to 8 hours. Cells in the penumbra may be salvaged by reperfusion or by drugs that prevent an extension of the infarction into the penumbral zone. Factors responsible for such an extension probably include acidosis, edema, K+/Ca++ transients, and inhibition of protein synthesis. Central to any discussion of the pathophysiology of ischemic lesions is energy depletion. This is because failure to maintain cellular adenosine triphosphate (ATP) levels leads to degradation of macromolecules of key importance to membrane and cytoskeletal integrity, to loss of ion homeostasis, involving cellular accumulation of Ca++, Na+, and Cl−, with osmotically obligated water, and to production of metabolic acids with a resulting decrease in intra- and extracellular pH. In all probability, loss of cellular calcium homeostasis plays an important role in the pathogenesis of ischemic cell damage. The resulting rise in the free cytosolic intracellular calcium concentration (Ca++) depends on both the loss of calcium pump function (due to ATP depletion), and the rise in membrane permeability to calcium. In ischemia, calcium influx occurs via multiple pathways. Some of the most important routes depend on activation of receptors by glutamate and associated excitatory amino acids released from depolarized presynaptic endings. However, ischemia also interferes with the intracellular sequestration and binding of calcium, thereby contributing to the rise in intracellular Ca++. A second key event in the ischemic tissue is activation of anaerobic glucolysis. The main reason for this activation is inhibition of mitochondrial metabolism by lack of oxygen; however, other factors probably contribute. For example, there is a complex interplay between loss of cellular calcium homeostasis and acidosis. On the one hand, a rise in intracellular Ca++ is apt to cause mitochondrial accumulation of calcium. This must interfere with ATP production and enhance anaerobic glucolysis. On the other hand, acidosis must interfere with calcium binding, thereby contributing to the rise in intracellular Ca++.
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Han, Xue Mei, Hong Tao Wei i Song Yan Liu. "Involvement of Erythropoietin Expression in Acupuncture Preconditioning-Induced Ischemic Tolerance". Advanced Materials Research 554-556 (lipiec 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 expressions of EPO could be detected in survival and necrotic neurons, glia as well as vascular endothelial cells. Focal cerebral ischemia promoted the expression of EPO. Significant enhanced EPO level was found in the ischemic peripheral zone after acupuncture preconditioning (P < 0.05). Conclusion Our results demonstrated that acupuncture preconditioning enhanced the expression of EPO in neurons, glia and vascular endothelial cells the ischemic peripheral zone, suggesting the involvement of EPO in acupuncture preconditioning-induced neuroprotection following focal cerebral ischemia. EPO may exert neuroprotective effects through promoting neurotrophic support and angiogenesis.
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Song, Siying, Hao Wu, Xunming Ji i Ran Meng. "The BE COOL Treatments (Batroxobin, oxygEn, Conditioning, and cOOLing): Emerging Adjunct Therapies for Ischemic Cerebrovascular Disease". Journal of Clinical Medicine 11, nr 20 (20.10.2022): 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 treatment goals for both arterial and venous ICDs include perfusion recovery, reduction of cerebral ischemic injury, and preservation of the neuronal integrity of the involved region as soon as possible; however, therapy based on the current guidelines for either acute ischemic events or chronic cerebral ischemia is not ideal because the recurrence rate of AIS or CVST is still very high. Therefore, this review discusses the neuroprotective effects of four novel potential ICD treatments with high translation rates, known as the BE COOL treatments (Batroxobin, oxygEn, Conditioning, and cOOLing), and subsequently analyzes how BE COOL treatments are used in clinical settings. The combination of batroxobin, oxygen, conditioning, and cooling may be a promising intervention for preserving ischemic tissues.
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Spetzler, Robert F. "Treatment of chronic cerebral ischemia". Surgical Neurology 23, nr 2 (luty 1985): 201. http://dx.doi.org/10.1016/0090-3019(85)90350-7.
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Ghosh, Nilanjan, Rituparna Ghosh, Zulfiqar A. Bhat, Vivekananda Mandal, Sitesh C. Bachar, Namsa D. Nima, Otimenyin O. Sunday i Subhash C. Mandal. "Advances in Herbal Medicine for Treatment of Ischemic Brain Injury". Natural Product Communications 9, nr 7 (lipiec 2014): 1934578X1400900. http://dx.doi.org/10.1177/1934578x1400900739.
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Ischemic brain injury is one of the leading causes of death worldwide and has attracted a lot of attention in the field of drug discovery. Cerebral ischemia is a complex pathological process involving a series of mechanisms, including generation of free radicals, oxidative stress, disruption of the membrane function, release of neurotransmitters and apoptosis. Thrombolytic therapy is the most effective therapeutic strategy, but the benefits are far from being absolute. Increased attention in the field of drug discovery has been focused on using natural compounds from traditional medicinal herbs for neuroprotection, which appears to be a promising therapeutic option for cerebral ischemia with minimal systemic adverse effects that could limit their long term use. The scenario calls for extensive investigations which can result in the development of lead molecules for neuroprotection in the future. In this context, the present review focuses on possible mechanisms underlying the beneficial effects of herbal drugs in patients with cerebral ischemic injury. Natural compounds have been demonstrated to have neurofunctional regulatory actions with antioxidative, anti-inflammatory, calcium antagonizing and anti-apoptotic activities. Among the several leads obtained from plant sources as potential neuroprotective agents, resveratrol, EGb761, curcumin and epigallocatechin-3-gallate have shown significant therapeutic benefits in cerebral ischemic conditions. However, ligustilide, tanshinone, scutellarin and shikonin are the few lead molecules which are under investigation for treatment of cerebral ischemia.
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Han, Xue Mei, Hong Tao Wei i Song Yan Liu. "Functional Role of HIF-1α in Hypoxic Preconditioning-Induced Neuroprotection against Focal Cerebral Ischemia". Advanced Materials Research 554-556 (lipiec 2012): 1762–67. http://dx.doi.org/10.4028/www.scientific.net/amr.554-556.1762.
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Objective To investigate the expression of HIF-1α after permenent focal cerebral ischemia and to explore the role of HIF-1α in hypoxic preconditioning-induced neuroprotection. Methods Rat focal cerebral ischemia model and hypoxic preconditioning models were established. Animals were randomly divided into four groups: healthy control, hypoxic preconditioning (3 h of 8% O2/92% N2 treatment), focal cerebral ischemia (6 h, 1 d, 3 d or 7 d) and hypoxic preconditioning + focal cerebral ischemia (6 h, 1 d, 3 d or 7 d). The expression of HIF-1α after different treatments was determined by histological examination, immunohistochemistry and in situ hybridization. Results The mRNA and protein expressions of HIF-1α could be detected in survival and necrotic neurons, glia as well as vascular endothelial cells. Hypoxic preconditioning significantly promoted the expression of HIF-1α after focal cerebral ischemia, especially in ischemic peripheral zone (P < 0.05).
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Dong, Chao, Jiawei Li, Ming Zhao, Lin Chen, Xiaochen Zhai, Lingling Song, Jin Zhao, Qiang Sun, Jie Wu i Xiaolu Xie. "Pharmacological Effect of Panax notoginseng Saponins on Cerebral Ischemia in Animal Models". BioMed Research International 2022 (4.08.2022): 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-adrenaline-induced systemic intravascular thrombosis in mice, thrombosis of carotid artery-jugular vein blood flow in the bypass of rats, and hypoxia tolerance in mice) were used to investigate the mechanisms underlying the actions of PNS on cerebral ischemia. The results indicated that (1) PNS improved neurological function and reduced the cerebral ischemia infraction area in MCAO rats; (2) PNS improved motor coordination function in rats with complete cerebral ischemia (blockade of four arteries), decreased Ca2+ levels, and ameliorated energy metabolism in the brains of ischemia rats; (3) PNS reduced thrombosis in common carotid artery-jugular vein blood flow in the bypass of rats; (4) PNS provided significant promise in antistroke hemiplegia and hypoxia tolerance in mice. In conclusion, PNS showed antagonistic effects on ischemic stroke, and pharmacological mechanisms are likely to be associated with the reduction of cerebral pathological damage, thrombolysis, antihypoxia, and improvement in the intracellular Ca2+ overload and cerebral energy metabolism.
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Ye, Hui, Zaiming Liu, Long Zhou i Qiang Cai. "Dynamic Observation of the Effect of L-Theanine on Cerebral Ischemia-Reperfusion Injury Using Magnetic Resonance Imaging under Mathematical Model Analysis". Journal of Healthcare Engineering 2021 (26.10.2021): 1–7. http://dx.doi.org/10.1155/2021/5679665.
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This study was to use the partial differential mathematical model to analyze the magnetic resonance imaging (MRI) images of cerebral ischemia-reperfusion injury (CIRI) and to dynamically observe the role of L-theanine in CIRI based on this. 30 patients with cerebral ischemia in a hospital in a certain area were selected and divided into a cerebral ischemia group and a L-theanine treatment group. The two groups of patients were examined by MRI within 48 hours, and the relative apparent diffusion coefficient (rADC) of the cerebral ischemic part of the patients was determined. The partial differential mathematical model was used for data processing to obtain the function of cerebral ischemia time and infarct area, and the data of patients in the cerebral ischemia group and L-theanine treatment group were compared and analyzed. The results showed that the partial differential mathematical model could effectively analyze the linear relationship between the rADC value and time in the treatment of CIRI using L-theanine. The rADC values of the four points of interest in the L-theanine treatment group all increased with time, and there was a positive correlation between the variables X and Y. In observing the efficacy indicators of L-theanine, the L-theanine treatment group showed a significant advantage in the neurospecific enolase (NSE) content compared with the cerebral ischemia group ( P < 0.01 ), and the neurological function score of the L-theanine treatment group gradually decreased and showed a statistically obvious difference on the 7th day of treatment ( P < 0.05 ). In summary, it was verified in this study that the role of L-theanine in the treatment of CIRI was of a great and positive significance for the subsequent treatment of patients with cerebral ischemia, providing reliable theoretical basis and data basis for clinical treatment of CIRI.
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Lopez, Mary S., Robert J. Dempsey i Raghu Vemuganti. "Resveratrol preconditioning induces cerebral ischemic tolerance but has minimal effect on cerebral microRNA profiles". Journal of Cerebral Blood Flow & Metabolism 36, nr 9 (21.07.2016): 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 cerebral microRNA levels, particularly those that target neuroprotective pathways. Therefore, we tested if resveratrol-mediated ischemic tolerance also alters microRNA expression with a goal to identify microRNAs that are amenable to manipulation to induce neuroprotection after cerebral ischemia. Hence, we tested the microRNA profiles in mouse brain following intraperitoneal administration of resveratrol that induced significant tolerance against transient focal ischemia. We analyzed microRNA profiles using microarrays from both Affymetrix and LC Sciences that contain probes for all known mouse microRNAs. The results show that there is no consistent change in any of the microRNAs tested between resveratrol and vehicle groups indicating that microRNAs play a minimal role in resveratrol-mediated cerebral ischemic tolerance.
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Li, Jin-hui, Jing Lu i Hong Zhang. "Functional Recovery after Scutellarin Treatment in Transient Cerebral Ischemic Rats: A Pilot Study with18F-Fluorodeoxyglucose MicroPET". Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/507091.
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Objective. To investigate neuroprotective effects of scutellarin (Scu) in a rat model of cerebral ischemia with use of18F-fluorodeoxyglucose (18F-FDG) micro positron emission tomography (microPET).Method. Middle cerebral artery occlusion was used to establish cerebral ischemia. Rats were divided into 5 groups: sham operation, cerebral ischemia-reperfusion untreated (CIRU) group, Scu-25 group (Scu 25 mg/kg/d), Scu-50 group (Scu 50 mg/kg/d), and nimodipine (10 mg/Kg/d). The treatment groups were given for 2 weeks. The therapeutic effects in terms of cerebral infarct volume, neurological deficit scores, and cerebral glucose metabolism were evaluated. Levels of vascular density factor (vWF), glial marker (GFAP), and mature neuronal marker (NeuN) were assessed by immunohistochemistry.Results. The neurological deficit scores were significantly decreased in the Scu-50 group compared to the CIRU group (P<0.001).18F-FDG accumulation in the ipsilateral cerebral infarction increased steadily over time in Scu-50 group compared with CIRU group (P<0.01) and Scu-25 group (P<0.01). Immunohistochemical analysis demonstrated Scu-50 enhanced neuronal maturation.Conclusion.18F-FDG microPET imaging demonstrated metabolic recovery after Scu-50 treatment in the rat model of cerebral ischemia. The neuroprotective effects of Scu on cerebral ischemic injury might be associated with increased regional glucose activity and neuronal maturation.
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Yano, Toshiyuki, Sakiko Anraku, Ryosuke Nakayama i Kazuo Ushijima. "Neuroprotective Effect of Urinary Trypsin Inhibitor against Focal Cerebral Ischemia–Reperfusion Injury in Rats". Anesthesiology 98, nr 2 (1.02.2003): 465–73. http://dx.doi.org/10.1097/00000542-200302000-00028.
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Background Acute inflammatory reactions cause neuronal damage in cerebral ischemia-reperfusion. Urinary trypsin inhibitor (UTI), a serine protease inhibitor, is cytoprotective against ischemia-reperfusion injury in the liver, intestine, kidney, heart, and lung through its antiinflammatory activity. Neuroprotective action of UTI on transient global cerebral ischemia has been documented. This is the first study to determine whether UTI is neuroprotective against transient focal cerebral ischemia. Methods Adult male Wistar rats were randomly assigned to the following treatment groups: 0.9% saline (control, n = 9); 100,000 U/kg UTI (n = 9); and 300,000 U/kg UTI (n = 9). Treatments were performed intravenously 10 min before right middle cerebral artery occlusion for 2 h and subsequent reperfusion. Ninety-six hours after the onset of reperfusion, the motor neurologic deficit and the cerebral infarct size were evaluated. Furthermore, immunohistochemical staining for myeloperoxidase and nitrotyrosine to count infiltrating neutrophils and nitrated cells, respectively, was performed on the brain sections. Results Infarct volume in the 300,000 U/kg UTI group was smaller than in the 100,000 U/kg UTI and saline control groups (P < 0.05). Treatment with 300,000 U/kg UTI showed a trend to improve neurologic outcome but did not reach statistical significance (P = 0.0693). The significant decrease in neutrophil infiltration was observed in the ischemic hemisphere treated with 300,000 U/kg UTI compared with saline control (P < 0.05). Nitrotyrosine deposition in the ischemic hemisphere was significantly reduced in the 300,000 U/kg UTI group compared with saline control and 100,000 U/kg UTI groups (P < 0.05). Conclusions Intravenous pretreatment with 300,000 U/kg UTI reduces focal ischemia-reperfusion injury in the rat brain, potentially opening a novel therapeutic avenue for the treatment of cerebral ischemia.
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Yagita, Yoshiki, Kazuo Kitagawa, Naoki Oyama, Toshiro Yukami, Akihiro Watanabe, Tsutomu Sasaki i Hideki Mochizuki. "Functional Deterioration of Endothelial Nitric Oxide Synthase after Focal Cerebral Ischemia". Journal of Cerebral Blood Flow & Metabolism 33, nr 10 (3.07.2013): 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 phosphorylation increased 6 hours after ischemia; however, there was an approximately 90% decrease in eNOS-Ser1177 phosphorylation observed 24 hours after ischemia that continued until at least 7 days after ischemia. Endothelial nitric oxide synthase monomer formation also increased 24 and 48 hours after ischemia ( P<0.05), and protein nitration progressed in parallel with monomerization. To assess the effect of a neuroprotective agent on eNOS dysfunction, we evaluated the effect of fasudil, a Rho-kinase inhibitor, on eNOS phosphorylation and dimerization. Postischemic treatment with fasudil suppressed lesion expansion and dephosphorylation and monomer formation of eNOS. In conclusion, functional deterioration of eNOS progressed after cerebral ischemia. Rho-kinase inhibitors can reduce ischemic lesion expansion as well as eNOS dysfunction in the ischemic brain.
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Pikis, Stylianos, Georgios Mantziaris, Vasileios Mamalis, Konstantinos Barkas, Antonios Tsanis, Stavroula Lyra, Kuriakos Karkoulias, Tigran Petrosyan i Eftychios Archontakis. "Diffusion weighted image documented cerebral ischemia in the postprocedural period following pipeline embolization device with shield technology treatment of unruptured intracranial aneurysms: a prospective, single center study". Journal of NeuroInterventional Surgery 12, nr 4 (26.09.2019): 407–11. http://dx.doi.org/10.1136/neurintsurg-2019-015363.
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ObjectiveAcute ischemic stroke and silent cerebral infarctions following pipeline embolization device (PED) treatment of intracranial aneurysms have been estimated to occur in 3–6% and in 50.9–90% of patients respectively. The PED with Shield technology (PED-Shield) incorporates a surface phosphorylcholine polymer to reduce the thrombogenicity of the implant. We sought to determine the incidence of diffusion weighted image (DWI) documented cerebral ischemia after PED-Shield treatment of unruptured intracranial aneurysms.MethodsThis prospective study involved a single center series of consecutive patients treated for an unruptured intracranial aneurysm with the PED-Shield. All participants underwent clinical evaluation on admission, after the procedure, at discharge, and 30 days following treatment. Brain MRI was obtained within 72 hours of the procedure. Ischemic lesions identified on DWI sequences where examined as to their number, size, and location in relation to the procedure.ResultsOver 12 months, 33 patients harboring 38 intracranial aneurysms were treated with the PED-Shield in 36 procedures. Neither mortality nor clinically evident ischemic events were noted in the 30 day postprocedural period. DWI documented, silent cerebral ischemia occurred in six patients (18.18%) after six procedures (16.66%). No statistically significant risk factors for postprocedural silent cerebral ischemia were identified.ConclusionWe demonstrated a reduced rate of silent cerebral infarcts following PED-Shield treatment of intracranial aneurysms than previously reported with other endovascular treatment modalities and with the previous device generations. Further research is necessary to evaluate our results and to identify methods to reduce the incidence of postprocedural cerebral ischemic events.
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Yu, Yong-Qiang, Lian-Cheng Liu, Fa-Cai Wang, Yan Liang, Da-Qin Cha, Jing-Jing Zhang, Yu-Jun Shen, Hai-Ping Wang, Shengyun Fang i Yu-Xian Shen. "Induction Profile of MANF/ARMET by Cerebral Ischemia and its Implication for Neuron Protection". Journal of Cerebral Blood Flow & Metabolism 30, nr 1 (23.09.2009): 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 apoptosis was determined by TUNEL staining; the expressions of proteins were measured by immunohistochemistry, immunofluorescent labeling, and Western blotting. ARMET was found to be extensively upregulated in ischemic regions in a time-dependent manner. The expression of ARMET was neuronal in all examined structures in response to the ischemic insult. We also found that ARMET expression is earlier and more sensitive to ischemic stimulation than C/EBP homologous protein (CHOP). ER stress agent tunicamycin induced ARMET and CHOP expressions in the primary cultured neurons. Treatment with recombinant human ARMET promoted neuron proliferation and prevented from neuron apoptosis induced by tunicamycin. These results suggest that cerebral ischemia-induced ARMET expression may be protective to the neurons.
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Savić, Tanja, Giuseppe Gambino, Vahid S. Bokharaie, Hamid R. Noori, Nikos K. Logothetis i Goran Angelovski. "Early detection and monitoring of cerebral ischemia using calcium-responsive MRI probes". Proceedings of the National Academy of Sciences 116, nr 41 (23.09.2019): 20666–71. http://dx.doi.org/10.1073/pnas.1908503116.
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Cerebral ischemia is one of the leading causes of mortality and disability in infants and adults and its timely diagnosis is essential for an efficient treatment. We present a methodology for fast detection and real-time monitoring of fluctuations of calcium ions associated with focal ischemia using a molecular functional MRI approach. We used a dinuclear paramagnetic gadolinium(III) complex chelate that changes MR image contrast through its reversible interaction with extracellular calcium ions, while applying a remote transient middle cerebral artery occlusion as a model for ischemic stroke. Our method sensitively recognizes the onset and follows the dynamics of the ischemic core and penumbra with submillimeter spatial and second-scale temporal resolution, thus paving the way for noninvasive monitoring and development of targeted treatment strategies for cerebral ischemia.
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Ahad, Mohamad Anuar, Kesevan Rajah Kumaran, Tiang Ning, Nur Izzati Mansor, Mohamad Azmeer Effendy, Thenmoly Damodaran, Kamilla Lingam i in. "Insights into the neuropathology of cerebral ischemia and its mechanisms". Reviews in the Neurosciences 31, nr 5 (28.07.2020): 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 pathophysiological mechanisms of these ischemic conditions. It is important to understand the pathophysiology of cerebral ischemia in order to identify therapeutic strategies for prevention and treatment. Here, we review the neuropathologies that are caused by cerebral ischemia and discuss the mechanisms that occur in cerebral ischemia such as reduction of cerebral blood flow, hippocampal damage, white matter lesions, neuronal cell death, cholinergic dysfunction, excitotoxicity, calcium overload, cytotoxic oedema, a decline in adenosine triphosphate (ATP), malfunctioning of Na+/K+-ATPase, and the blood-brain barrier breakdown. Altogether, the information provided can be used to guide therapeutic strategies for cerebral ischemia.
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Jacewicz, Michael, Steve Brint, Jody Tanabe, Xing-Je Wang i William A. Pulsinelli. "Nimodipine Pretreatment Improves Cerebral Blood Flow and Reduces Brain Edema in Conscious Rats Subjected to Focal Cerebral Ischemia". Journal of Cerebral Blood Flow & Metabolism 10, nr 6 (listopad 1990): 903–13. http://dx.doi.org/10.1038/jcbfm.1990.147.
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The effect of nimodipine pretreatment on CBF and brain edema was studied in conscious rats subjected to 2.5 h of focal cortical ischemia. An infusion of nimodipine (2 μg/kg/min i.v.) or its vehicle, polyethylene glycol 400, was begun 2 h before the ischemic interval and was continued throughout the survival period. Under brief halothane anesthesia, the animals' right middle cerebral and common carotid arteries were permanently occluded, and 2.5 h later, they underwent a quantitative CBF study ([14C]iodoantipyrine autoradiography followed by Quantimet 970 image analysis). Nimodipine treatment improved blood flow to the middle cerebral artery territory without evidence of a “vascular steal” and reduced the volume of the ischemic core (cortex with CBF of < 25 ml/100 g/min) and accompanying edema by ∼50% when compared with controls (p = 0.006 and 0.0004, respectively). Mild hypotension induced by nimodipine did not aggravate the ischemic insult. The ischemic core volumes, however, were 50–75% smaller than the 24-h infarct volumes generated in a similar paradigm that demonstrated 20–30% infarct reduction with continuous nimodipine treatment. These results suggest that nimodipine pretreatment attenuates the severity of early focal cerebral ischemia, but that with persistent ischemia, cortex surrounding the ischemic core undergoes progressive infarction and the early benefit of nimodipine treatment is only partly preserved.
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Jacewicz, Michael, Steve Brint, Jody Tanabe i William A. Pulsinelli. "Continuous Nimodipine Treatment Attenuates Cortical Infarction in Rats Subjected to 24 Hours of Focal Cerebral Ischemia". Journal of Cerebral Blood Flow & Metabolism 10, nr 1 (styczeń 1990): 89–96. http://dx.doi.org/10.1038/jcbfm.1990.11.
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Focal cerebral infarction and edema were measured in rats (Wistar, Fisher 344, and spontaneously hypertensive strains) pretreated with nimodipine (2 μg/kg/min i.v.) or its vehicle and subjected to the tandem occlusion of the middle cerebral and common carotid arteries. Animals awoke from anesthesia 10–15 min after onset of ischemia and continued to receive treatment over a 24-h survival period. Cortical infarction and edema were quantified by image analysis of frozen brain sections processed for histology. Nimodipine-treated rats developed 20–60% smaller cortical infarct volumes than controls (p < 0.002). Cortical edema was reduced proportionately to the decrease in infarct volume and constituted ∼36% of the infarct volume. Nimodipine caused a mild hypotensive response that did not aggravate ischemic brain damage. The results indicate that continuous nimodipine treatment, started before induction of focal cerebral ischemia, can attenuate ischemic brain damage and edema as late as 24 h after the onset of ischemia.
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Sun, Jui-Ming, Ting-Lin Yen, Jing-Shiun Jan, Pharaoh Fellow Mwale, Ruei-Dun Teng, Rajeev Taliyan, Cheng-Ta Hsieh i Chih-Hao Yang. "Advances in Antibody-Based Therapeutics for Cerebral Ischemia". Pharmaceutics 15, nr 1 (31.12.2022): 145. http://dx.doi.org/10.3390/pharmaceutics15010145.
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Cerebral ischemia is an acute disorder characterized by an abrupt reduction in blood flow that results in immediate deprivation of both glucose and oxygen. The main types of cerebral ischemia are ischemic and hemorrhagic stroke. When a stroke occurs, several signaling pathways are activated, comprising necrosis, apoptosis, and autophagy as well as glial activation and white matter injury, which leads to neuronal cell death. Current treatments for strokes include challenging mechanical thrombectomy or tissue plasminogen activator, which increase the danger of cerebral bleeding, brain edema, and cerebral damage, limiting their usage in clinical settings. Monoclonal antibody therapy has proven to be effective and safe in the treatment of a variety of neurological disorders. In contrast, the evidence for stroke therapy is minimal. Recently, Clone MTS510 antibody targeting toll-like receptor-4 (TLR4) protein, ASC06-IgG1 antibody targeting acid sensing ion channel-1a (ASIC1a) protein, Anti-GluN1 antibodies targeting N-methyl-D-aspartate (NMDA) receptor associated calcium influx, GSK249320 antibody targeting myelin-associated glycoprotein (MAG), anti-High Mobility Group Box-1 antibody targeting high mobility group box-1 (HMGB1) are currently under clinical trials for cerebral ischemia treatment. In this article, we review the current antibody-based pharmaceuticals for neurological diseases, the use of antibody drugs in stroke, strategies to improve the efficacy of antibody therapeutics in cerebral ischemia, and the recent advancement of antibody drugs in clinical practice. Overall, we highlight the need of enhancing blood–brain barrier (BBB) penetration for the improvement of antibody-based therapeutics in the brain, which could greatly enhance the antibody medications for cerebral ischemia in clinical practice.
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Vongsfak, Jirapong, Wasana Pratchayasakul, Nattayaporn Apaijai, Tanat Vaniyapong, Nipon Chattipakorn i Siriporn C. Chattipakorn. "The Alterations in Mitochondrial Dynamics Following Cerebral Ischemia/Reperfusion Injury". Antioxidants 10, nr 9 (30.08.2021): 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 demonstrated that an imbalance in mitochondrial dynamics after cerebral ischemia, with or without reperfusion injury, plays an important role in the regulation of cell survival and infarct area size. Mitochondrial dysmorphology/dysfunction and inflammatory processes also occur after cerebral ischemia. Knowledge surrounding the mechanisms involved in the imbalance in mitochondrial dynamics following cerebral ischemia with or without reperfusion injury would help in the prevention or treatment of the adverse effects of cerebral injury. Therefore, this review aims to summarize and discuss the roles of mitochondrial dynamics, mitochondrial function, and inflammatory processes in cerebral ischemia with or without reperfusion injury from in vitro and in vivo studies. Any contradictory findings are incorporated and discussed.
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Packard, Amy E. B., Jason C. Hedges, Frances R. Bahjat, Susan L. Stevens, Michael J. Conlin, Andres M. Salazar i Mary P. Stenzel-Poore. "Poly-IC Preconditioning Protects against Cerebral and Renal Ischemia-Reperfusion Injury". Journal of Cerebral Blood Flow & Metabolism 32, nr 2 (16.11.2011): 242–47. http://dx.doi.org/10.1038/jcbfm.2011.160.
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Preconditioning induces ischemic tolerance, which confers robust protection against ischemic damage. We show marked protection with polyinosinic polycytidylic acid (poly-IC) preconditioning in three models of murine ischemia-reperfusion injury. Poly-IC preconditioning induced protection against ischemia modeled in vitro in brain cortical cells and in vivo in models of brain ischemia and renal ischemia. Further, unlike other Toll-like receptor (TLR) ligands, which generally induce significant inflammatory responses, poly-IC elicits only modest systemic inflammation. Results show that poly-IC is a new powerful prophylactic treatment that offers promise as a clinical therapeutic strategy to minimize damage in patient populations at risk of ischemic injury.
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Smirnov, Ivan E., A. A. Stepanov, L. D. Shakina, I. A. Belyaeva, E. P. Bombardirova i A. G. Kucherenko. "Neurologic manifestations of cerebral ischemia in infants at 1 year of age". Russian Pediatric Journal 19, nr 5 (30.04.2019): 274–82. http://dx.doi.org/10.18821/1560-9561-2016-19-5-274-282.
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Hypoxic-ischemic brain damage of the newborn infant to date is the one of the major problems in neonatology. The comprehensive clinical, laboratory and neurological examination of newborns of different gestational ages with perinatal CNS disorder was executed with the use of informative diagnostic technologies. Structural and functional disorders caused by cerebral ischemia, were established to be accompanied by significant changes in brain activity, the severity of which increases with decreasing gestational age of newborns. Certain concentrations of plasma factors of hemostasis in newborns were shown to be markers of the severity of cerebral ischemia and efficiency of complex neuroprotective therapy. Positive neurotrophic effects of gliatilin in the treatment of infants with cerebral ischemia were established to manifest by normalization of the clinical state, neurological symptoms and stabilization of plasma hemostasis, which determined the rate of regenerative treatment of ischemic brain injuries.
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Zhang, Chan, Luming Zhen, Zongping Fang, Liang Yu, Yuanyuan Zhang, Haidong Wei, Junfeng Jia i Shiquan Wang. "Adiponectin Treatment Attenuates Cerebral Ischemia-Reperfusion Injury through HIF-1α-Mediated Antioxidation in Mice". Oxidative Medicine and Cellular Longevity 2021 (14.07.2021): 1–16. http://dx.doi.org/10.1155/2021/5531048.
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Adiponectin (ADPN) plays an important role in cerebral ischemia-reperfusion injury. Although previous studies have confirmed that ADPN pretreatment has a protective effect on ischemic stroke, the therapeutic effect of ADPN on ischemic stroke and the underlying mechanism are still unclear. In order to clarify these questions, focal transient cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in mice and ADPN was administered for three times at 6 h, 24 h, and 48 h after reperfusion. Meanwhile, a virus-delivered HIF-1α siRNA was used before ADPN administration. The infarct volume, neurological score, cellular apoptosis, and oxidative stress were assessed at 72 h after reperfusion. The long-term outcome of mice after stroke was recorded as well. The results indicated that ADPN treatment reduced the infarct volume ( P = 0.032 ), neurological deficits ( P = 0.047 ), cellular apoptosis ( P = 0.041 ), and oxidative responses ( P = 0.031 ) at 72 h after MCAO. Moreover, ADPN increased both the protein level and transcriptional activity of HIF-1α as evidenced by the transcription levels of VEGF ( P = 0.046 ) and EPO ( P = 0.043 ) at 72 h after MCAO. However, knockdown of HIF-1α partially reversed the antioxidant and treatment effect of ADPN after cerebral ischemia. In the observation of long-term outcome after ADPN treatment, it demonstrated that ADPN not only prevented the cerebral atrophy ( P = 0.031 ) and the neurological function decline ( P = 0.048 ), but also promoted angiogenesis ( P = 0.028 ) after stroke. In conclusion, our findings suggest that ADPN is effective in treatment of ischemic stroke which could be attributed to the increased antioxidant capacity regulated by HIF-1α.
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Marteau, Léna, Samuel Valable, Didier Divoux, Simon A. Roussel, Omar Touzani, Eric T. MacKenzie, Myriam Bernaudin i Edwige Petit. "Angiopoietin-2 is Vasoprotective in the Acute Phase of Cerebral Ischemia". Journal of Cerebral Blood Flow & Metabolism 33, nr 3 (5.12.2012): 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 VEGF, in the acute phase of cerebral ischemia. The effect of these angiogenic factors on the ischemic lesion volume was evaluated by magnetic resonance imaging. We observed that timely administration of VEGF exacerbates ischemic damage. In contrast, Ang2 decreases the ischemic volume and this beneficial effect is maintained in the presence of VEGF. This investigation reports, for the first time, a protective role of Ang2 following cerebral ischemia, an action associated with a reduced BBB permeability. We propose that Ang2 represents a pertinent molecular target for the treatment of cerebral ischemia since acute brain damage may be limited by a pharmacological protection of the vascular compartment.
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Armstrong, SL. "Cerebral vasospasm: early detection and intervention". Critical Care Nurse 14, nr 4 (1.08.1994): 33–37. http://dx.doi.org/10.4037/ccn1994.14.4.33.
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Many patients survive SAH with minimal neurologic deficits but are at risk for developing further neurologic insult from ischemia resulting from cerebral vasospasm. Nursing care of the patient experiencing vasospasm is challenging. The nurse who is knowledgeable about the signs and symptoms of cerebral ischemia and necessity for continually reviewing the patient's neurologic status can initiate prompt treatment to prevent further ischemic damage. Recognition of this critical problem is the first step toward combating its ominous effects.
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Du, Fang, Tao Tang, Qingzhu Li i Jiaxin Liu. "Fyn Signaling in Ischemia-Reperfusion Injury: Potential and Therapeutic Implications". Mediators of Inflammation 2022 (15.09.2022): 1–10. http://dx.doi.org/10.1155/2022/9112127.
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Ischemic stroke caused by arterial occlusion is the most common type of stroke and is one of the leading causes of disability and death, with the incidence increasing each year. Fyn is a nonreceptor tyrosine kinase belonging to the Src family of kinases (SFKs), which is related to many normal and pathological processes of the nervous system, including neurodevelopment and disease progression. In recent years, more and more evidence suggests that Fyn may be closely related to cerebral ischemia-reperfusion, including energy metabolism disorders, excitatory neurotoxicity, intracellular calcium homeostasis, free radical production, and the activation of apoptotic genes. This paper reviews the role of Fyn in the pathological process of cerebral ischemia-reperfusion, including neuroexcitotoxicity and neuroinflammation, to explore how Fyn affects specific signal cascades and leads to cerebral ischemia-reperfusion injury. In addition, Fyn also promotes the production of superoxide and endogenous NO, so as to quickly react to produce peroxynitrite, which may also mediate cerebral ischemia-reperfusion injury, which is discussed in this paper. Finally, we revealed the treatment methods related to Fyn inhibitors and discussed its potential as a clinical treatment for ischemic stroke.
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Lim, Songhyun, Tae Jung Kim, Young-Ju Kim, Cheesue Kim, Sang-Bae Ko i Byung-Soo Kim. "Senolytic Therapy for Cerebral Ischemia-Reperfusion Injury". International Journal of Molecular Sciences 22, nr 21 (4.11.2021): 11967. http://dx.doi.org/10.3390/ijms222111967.
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Ischemic stroke is one of the leading causes of death, and even timely treatment can result in severe disabilities. Reperfusion of the ischemic stroke region and restoration of the blood supply often lead to a series of cellular and biochemical consequences, including generation of reactive oxygen species (ROS), expression of inflammatory cytokines, inflammation, and cerebral cell damage, which is collectively called cerebral ischemia-reperfusion (IR) injury. Since ROS and inflammatory cytokines are involved in cerebral IR injury, injury could involve cellular senescence. Thus, we investigated whether senolytic therapy that eliminates senescent cells could be an effective treatment for cerebral IR injury. To determine whether IR induces neural cell senescence in vitro, astrocytes were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R). OGD/R induced astrocyte senescence and senescent cells in OGD/R-injured astrocytes were effectively eliminated in vitro by ABT263, a senolytic agent. IR in rats with intraluminal middle cerebral artery occlusion induced cellular senescence in the ischemic region. The senescent cells in IR-injured rats were effectively eliminated by intravenous injections of ABT263. Importantly, ABT263 treatment significantly reduced the infarct volume and improved neurological function in behavioral tests. This study demonstrated, for the first time, that senolytic therapy has therapeutic potential for cerebral IR injury.
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Pu, Fengling, Kenichi Mishima, Nobuaki Egashira, Yuki Akiyoshi, An-Xin Liu, Kazunori Sano, Keiichi Irie i in. "Post-ischemic Treatment with Toki-Shakuyaku-San (Tang-Gui-Shao-Yao-San) Prevents the Impairment of Spatial Memory Induced by Repeated Cerebral Ischemia in Rats". American Journal of Chinese Medicine 33, nr 03 (styczeń 2005): 475–89. http://dx.doi.org/10.1142/s0192415x05003077.
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Previously we have reported that Toki-shakuyaku-san (TSS) ameliorated the impairment of spatial memory induced by single cerebral ischemia (1 × 10 minutes ) and scopolamine, a muscarinic receptor antagonist. In this experiment, we studied the effect of TSS on repeated cerebral ischemia (2 × 10 minutes , 1-hour interval) induced impairment of spatial memory and neuronal injury in rats. The 8-day post-ischemic treatment with TSS (30–300 mg/kg) was administered p.o. once per day. TSS dose-dependently prevented the impairment of spatial memory, neuronal death and TUNEL positive cells induced by repeated cerebral ischemia. In order to determine the mechanism of TSS, we also studied the effect of TSS on GluR2 mRNA, one of the glutamate α-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) receptor subunits. Repeated cerebral ischemia significantly decreased GluR2 flop mRNA at 1 and 3 days after the occlusion. TSS (300 mg/kg) significantly suppressed the decrease in GluR2 flop at 3 days after repeated cerebral ischemia. These results suggested that the TSS has neuroprotective action which may be indirectly mediated by the AMPA receptor, and TSS may be beneficial for the treatment of cerebrovascular dementia.
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Godínez-Rubí, Marisol, Argelia E. Rojas-Mayorquín i Daniel Ortuño-Sahagún. "Nitric Oxide Donors as Neuroprotective Agents after an Ischemic Stroke-Related Inflammatory Reaction". Oxidative Medicine and Cellular Longevity 2013 (2013): 1–16. http://dx.doi.org/10.1155/2013/297357.
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Cerebral ischemia initiates a cascade of detrimental events including glutamate-associated excitotoxicity, intracellular calcium accumulation, formation of Reactive oxygen species (ROS), membrane lipid degradation, and DNA damage, which lead to the disruption of cellular homeostasis and structural damage of ischemic brain tissue. Cerebral ischemia also triggers acute inflammation, which exacerbates primary brain damage. Therefore, reducing oxidative stress (OS) and downregulating the inflammatory response are options that merit consideration as potential therapeutic targets for ischemic stroke. Consequently, agents capable of modulating both elements will constitute promising therapeutic solutions because clinically effective neuroprotectants have not yet been discovered and no specific therapy for stroke is available to date. Because of their ability to modulate both oxidative stress and the inflammatory response, much attention has been focused on the role of nitric oxide donors (NOD) as neuroprotective agents in the pathophysiology of cerebral ischemia-reperfusion injury. Given their short therapeutic window, NOD appears to be appropriate for use during neurosurgical procedures involving transient arterial occlusions, or in very early treatment of acute ischemic stroke, and also possibly as complementary treatment for neurodegenerative diseases such as Parkinson or Alzheimer, where oxidative stress is an important promoter of damage. In the present paper, we focus on the role of NOD as possible neuroprotective therapeutic agents for ischemia/reperfusion treatment.
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Liang, Jia, Zhifeng Qi, Wenlan Liu, Peng Wang, Wenjuan Shi, Wen Dong, Xunming Ji, Yumin Luo i Ke Jian Liu. "Normobaric Hyperoxia Slows Blood–Brain Barrier Damage and Expands the Therapeutic Time Window for Tissue-Type Plasminogen Activator Treatment in Cerebral Ischemia". Stroke 46, nr 5 (maj 2015): 1344–51. http://dx.doi.org/10.1161/strokeaha.114.008599.
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Background and Purpose— Prolonged ischemia causes blood–brain barrier (BBB) damage and increases the incidence of neurovasculature complications secondary to reperfusion. Therefore, targeting ischemic BBB damage pathogenesis is critical to reducing neurovasculature complications and expanding the therapeutic time window of tissue-type plasminogen activator (tPA) thrombolysis. This study investigates whether increasing cerebral tissue P O 2 through normobaric hyperoxia (NBO) treatment will slow the progression of BBB damage and, thus, improve the outcome of delayed tPA treatment after cerebral ischemia. Methods— Rats were exposed to NBO (100% O 2 ) or normoxia (21% O 2 ) during 3-, 5-, or, 7-hour middle cerebral artery occlusion. Fifteen minutes before reperfusion, tPA was continuously infused to rats for 30 minutes. Neurological score, mortality rate, and BBB permeability were determined. Matrix metalloproteinase-9 was measured by gelatin zymography and tight junction proteins (occludin and cluadin-5) by Western blot in the isolated cerebral microvessels. Results— NBO slowed the progression of ischemic BBB damage pathogenesis, evidenced by reduced Evan blue leakage, smaller edema, and hemorrhagic volume in NBO-treated rats. NBO treatment reduced matrix metalloproteinase-9 induction and the loss of tight junction proteins in ischemic cerebral microvessels. NBO-afforded BBB protection was maintained during tPA reperfusion, resulting in improved neurological functions, significant reductions in brain edema, hemorrhagic volume, and mortality rate, even when tPA was given after prolonged ischemia (7 hours). Conclusions— Early NBO treatment slows ischemic BBB damage pathogenesis and significantly improves the outcome of delayed tPA treatment, providing new evidence supporting NBO as an effective adjunctive therapy to extend the time window of tPA thrombolysis for ischemic stroke.
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Lu, Hongwei, Yaqin Meng, Xinrui Han i Wei Zhang. "ADAM8 Activates NLRP3 Inflammasome to Promote Cerebral Ischemia-Reperfusion Injury". Journal of Healthcare Engineering 2021 (16.12.2021): 1–14. http://dx.doi.org/10.1155/2021/3097432.
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Stroke is the leading cause of death and disability in humans. Strokes are classified as either ischemic or hemorrhagic. Ischemic stroke accounts for 70–80% of the cases. Inflammation is a key factor in ischemic brain injury. Studies have shown that inflammatory response induced by NLRP3 inflammasome is one of the root causes of brain damage in mice with cerebral ischemia. However, its specific mechanism in cerebral ischemia is still unclear. ADAM8 (a disintegrin and metalloproteases 8) is a transmembrane protein with different functions. It plays an important role in tumors and neuroinflammation-related diseases. However, the role and molecular mechanism of ADAM8 in cerebral ischemia injury are still unclear. This study aims to evaluate the role of ADAM8 in cerebral ischemic injury and explore its signal transduction mechanism. This experiment shows that ADAM8 can significantly cause neurological deficits in MCAO mice and can substantially cause ipsilateral cerebral edema and cerebral infarction in MCAO mice. In addition, ADAM8 can significantly induce cortical cell apoptosis in MCAO mice, leading to the loss of neurons and the expression of proinflammatory factors COX2, iNOS, TNFα, and IL-6. Importantly, we confirmed that ADAM8 mediates the inflammatory response by promoting the activation of NLRP3 inflammasome, microglia, and astrocytes. These results indicate that ADAM8 may be a candidate drug target for the prevention and treatment of the cerebral ischemic injury.
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Bullock, R., D. I. Graham, S. Swanson i J. McCulloch. "Neuroprotective Effect of the AMPA Receptor Antagonist LY-293558 in Focal Cerebral Ischemia in the Cat". Journal of Cerebral Blood Flow & Metabolism 14, nr 3 (maj 1994): 466–71. http://dx.doi.org/10.1038/jcbfm.1994.57.
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The effects of the glutamate α-amino-3-hydroxy 5-methyl-4-isoxazole propionate (AMPA) receptor antagonist LY-293558 in reducing ischemic brain damage have been assessed in halothane-anesthetized cats. Focal cerebral ischemia was produced by permanent occlusion of one middle cerebral artery, and the animals were killed 6 h later. The amount of early irreversible ischemic damage was assessed at 16 predetermined stereotactic planes by an observer blinded to treatment paradigm employed. Treatment with LY-293558 (15 mg/kg i.v., plus infusion of 7 mg/kg/h) initiated 30 min prior to middle cerebral artery occlusion reduced significantly (p < 0.02) the volume of ischemic damage (from 3,423 ± 212 mm3 of the cerebral hemisphere in vehicle-treated cats to 2,822 ± 569 mm3 in LY-293558-treated cats). The present data demonstrate that an AMPA receptor antagonist can reduce focal ischemic damage in a gyrencephalic species in which key physiological variables have been controlled and monitored throughout the postischemic period. These data provide additional support for the clinical evaluation of AMPA receptor antagonists in focal cerebral ischemia in humans.
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Fan, Yan-Ying, Zhe Shen, Ping He, Lei Jiang, Wei-wei Hou, Yao Shen, Xiang-Nan Zhang, Wei-Wei Hu i Zhong Chen. "A Novel Neuroprotective Strategy for Ischemic Stroke: Transient Mild Acidosis Treatment by CO2 Inhalation at Reperfusion". Journal of Cerebral Blood Flow & Metabolism 34, nr 2 (6.11.2013): 275–83. http://dx.doi.org/10.1038/jcbfm.2013.193.
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Acidosis is one of the key components in cerebral ischemic postconditioning that has emerged recently as an endogenous strategy for neuroprotection. We set out to test whether acidosis treatment at reperfusion can protect against cerebral ischemia/reperfusion injury. Adult male C57BL/6 J mice were subjected to 60-minute middle cerebral arterial occlusion followed by 24-hour reperfusion. Acidosis treatment by inhaling 10%, 20%, or 30% CO2 for 5 or 10 minutes at 5, 50, or 100 minutes after reperfusion was applied. Our results showed that inhaling 20% CO2 for 5 minutes at 5 minutes after reperfusion-induced optimal neuroprotection, as revealed by reduced infarct volume. Attenuating brain acidosis with NaHCO3 significantly compromised the acidosis or ischemic postconditioning-induced neuroprotection. Consistently, both acidosis-treated primary cultured cortical neurons and acute corticostriatal slices were more resistant to oxygen–glucose deprivation/reperfusion insult. In addition, acidosis inhibited ischemia/reperfusion-induced apoptosis, caspase-3 expression, cytochrome c release to cytoplasm, and mitochondrial permeability transition pore (mPTP) opening. The neuroprotection of acidosis was inhibited by the mPTP opener atractyloside both in vivo and in vitro. Taken together, these findings indicate that transient mild acidosis treatment at reperfusion protects against cerebral ischemia/reperfusion injury. This neuroprotection is likely achieved, at least partly, by inhibiting mPTP opening and mitochondria-dependent apoptosis.
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Regli, Luca, Mark C. Held, Robert E. Anderson i Fredric B. Meyer. "Nitric Oxide Synthase Inhibition by L-NAME Prevents Brain Acidosis during Focal Cerebral Ischemia in Rabbits". Journal of Cerebral Blood Flow & Metabolism 16, nr 5 (wrzesień 1996): 988–95. http://dx.doi.org/10.1097/00004647-199609000-00024.
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This experiment examined the effects of nitric oxide (NO) synthase inhibition on brain intracellular pH, regional cortical blood flow, and NADH fluorescence before and during 3 h of focal cerebral ischemia using in vivo fluorescence imaging. Thirty fasted rabbits under 1% halothane were divided into four treatment groups receiving Nω-nitro-L-arginine methyl ester (L-NAME) intravenously at 20 min prior to ischemia (0.1, I, and 10 mg/kg and 1 mg/kg + 5 mg/kg L-arginine) and two control groups (nonischemic and ischemic). In ischemic controls, brain pHi declined to 6.73 ± 0.03 at 30 min and remained acidotic through the remainder of the ischemic period. In the 0.1 mg/kg group, brain pHi fell after 30 min of ischemia to 6.76 ± 0.05 ( p < 0.05), but then improved progressively despite occlusion. In the 1 mg/kg group, brain pHi remained normal despite middle cerebral artery (MCA) occlusion. In the 10 mg/kg group and in the combined L-NAME + L-arginine group, pHi fell after 30 min of ischemia to 6.81 ± 0.03 ( p < 0.05) and remained acidotic. During occlusion, regional cortical blood flow dropped in a dose-dependent manner. After 3 h of ischemia, regional cortical blood flow was 33.9 ± 10.9 and 25.1 ± 8.9 ml/100 g/min at doses of 0.1 and 10.0 mg/kg, respectively. L-NAME treatment did not significantly alter the increased NADH fluorescence that accompanied occlusion. This study shows that L-NAME can prevent intracellular brain acidosis during focal cerebral ischemia independent from regional cortical blood flow changes. This experiment suggests that NO is involved in pHi regulation during focal cerebral ischemia.
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Schulz, Mette K., Lars Peter Wang, Mogens Tange i Per Bjerre. "Cerebral microdialysis monitoring: determination of normal and ischemic cerebral metabolisms in patients with aneurysmal subarachnoid hemorrhage". Journal of Neurosurgery 93, nr 5 (listopad 2000): 808–14. http://dx.doi.org/10.3171/jns.2000.93.5.0808.
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Object. The success of treatment for delayed cerebral ischemia is time dependent, and neuronal monitoring methods that can detect early subclinical levels of cerebral ischemia may improve overall treatment results. Cerebral microdialysis may represent such a method. The authors' goal was to characterize patterns of markers of energy metabolism (glucose, pyruvate, and lactate) and neuronal injury (glutamate and glycerol) in patients with subarachnoid hemorrhage (SAH), in whom ischemia was or was not suspected.Methods. By using low-flow intracerebral microdialysis monitoring, central nervous system extracellular fluid concentrations of glucose, pyruvate, lactate, glutamate, and glycerol were determined in 46 patients suffering from poor-grade SAH. The results in two subgroups were analyzed: those patients with no clinical or radiological signs of cerebral ischemia (14 patients) and those who succumbed to brain death (five patients).Significantly lower levels of energy substrates and significantly higher levels of lactate and neuronal injury markers were observed in patients with severe and complete ischemia when compared with patients without symptoms of ischemia (glucose 0 compared with 2.12 ± 0.15 mmol/L; pyruvate 0 compared with 151 ± 11.5 µmol; lactate 6.57 ± 1.07 compared with 3.06 ± 0.32 mmol/L; glycerol 639 ± 91 compared with 81.6 ± 12.4 µmol; and glutamate 339 ± 53.4 compared with 14 ± 3.33 µmol). Immediately after catheter placement, glutamate concentrations declined over the first 4 to 6 hours to reach stable values. The remaining parameters exhibited stable values after 1 to 2 hours.Conclusions. The results confirm that intracerebral microdialysis monitoring of patients with SAH can be used to detect patterns of cerebral ischemia. The wide range from normal to severe ischemic values calls for additional studies to characterize further incomplete and possible subclinical levels of ischemia.
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Schweizer, Sophie, Andreas Meisel i Stefanie Märschenz. "Epigenetic Mechanisms in Cerebral Ischemia". Journal of Cerebral Blood Flow & Metabolism 33, nr 9 (12.06.2013): 1335–46. http://dx.doi.org/10.1038/jcbfm.2013.93.
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Treatment efficacy for ischemic stroke represents a major challenge. Despite fundamental advances in the understanding of stroke etiology, therapeutic options to improve functional recovery remain limited. However, growing knowledge in the field of epigenetics has dramatically changed our understanding of gene regulation in the last few decades. According to the knowledge gained from animal models, the manipulation of epigenetic players emerges as a highly promising possibility to target diverse neurologic pathologies, including ischemia. By altering transcriptional regulation, epigenetic modifiers can exert influence on all known pathways involved in the complex course of ischemic disease development. Beneficial transcriptional effects range from attenuation of cell death, suppression of inflammatory processes, and enhanced blood flow, to the stimulation of repair mechanisms and increased plasticity. Most striking are the results obtained from pharmacological inhibition of histone deacetylation in animal models of stroke. Multiple studies suggest high remedial qualities even upon late administration of histone deacetylase inhibitors (HDACi). In this review, the role of epigenetic mechanisms, including histone modifications as well as DNA methylation, is discussed in the context of known ischemic pathways of damage, protection, and regeneration.
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Iwata, Naohiro, Hiroko Takayama, Meiyan Xuan, Shinya Kamiuchi, Hirokazu Matsuzaki, Mari Okazaki i Yasuhide Hibino. "Effects of Etanercept against Transient Cerebral Ischemia in Diabetic Rats". BioMed Research International 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/189292.
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Diabetes mellitus is known to exacerbate acute cerebral ischemic injury. Previous studies have demonstrated that infarction volumes caused by transient cerebral ischemia were greater in diabetic rats than in nondiabetic rats. Tumor necrosis factor-α(TNF-α) is a proinflammatory protein produced in the brain in response to cerebral ischemia that promotes apoptosis. Etanercept (ETN), a recombinant TNF receptor (p75)-Fc fusion protein, competitively inhibits TNF-α. Therefore, we evaluated the neuroprotective effects of chronic or acute treatment with ETN on cerebral injury caused by middle cerebral artery occlusion/reperfusion (MCAO/Re) in rats with streptozotocin-induced diabetes. Furthermore, we evaluated the effects of ETN against the apoptosis and myeloperoxidase activity. Single administration of ETN before MCAO significantly suppressed exacerbation of cerebral damage in nondiabetic rats, as assessed by infarct volume. In contrast, the diabetic state markedly aggravated MCAO/Re-induced cerebral damage despite ETN treatment within 24 h before MCAO. However, the damage was improved by repeated administration of ETN at 900 μg/kg/daily in rats in an induced diabetic state. These results suggested that repeated administration of ETN can prevent exacerbation of cerebral ischemic injury in the diabetic state and is mainly attributed to anti-inflammatory effects.
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Zakharov, V. V., V. V. Grinyuk, N. V. Vakhnina i E. Yu Kalimeeva. "Treatment of comorbid patients with chronic brain ischemia and vertebrogenic pain syndromes". Medical Council, nr 9 (12.06.2019): 15–20. http://dx.doi.org/10.21518/2079-701x-2019-9-15-20.
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Chronic brain ischemia and chronic pain both appear to be an extremely wide-spread disease. The reasons of widespread comorbidity of ischemic brain disease and chronic pain are common risk factors: old age, decrease of physical activity, syndrome of systemic inflammation and emotional disturbances. Treatment of patients with cerebrovascular diseases and chronic pain should influence common mechanisms of these disorders. Correction of microcirculatory disturbances pays particular important role, because this is the mechanism not only of chronic cerebral ischemia but compressive-ischemic radiculo- and neuropathy also.
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ISHIKAWA, Tatsuya. "Advancement in Treatment for Ischemic Cerebral Ischemia in the Acute Stage". Surgery for Cerebral Stroke 33, nr 2 (2005): 85–88. http://dx.doi.org/10.2335/scs.33.85.
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Koerner, Ines P., Matthias Gatting, Ruediger Noppens, Oliver Kempski i Ansgar M. Brambrink. "Induction of Cerebral Ischemic Tolerance by Erythromycin Preconditioning Reprograms the Transcriptional Response to Ischemia and Suppresses Inflammation". Anesthesiology 106, nr 3 (1.03.2007): 538–47. http://dx.doi.org/10.1097/00000542-200703000-00019.
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Background A single dose of the macrolide antibiotic erythromycin can induce tolerance against cerebral ischemia in vivo (pharmacologic preconditioning). This study identified potential mechanisms of tolerance induction by assessing effects of erythromycin preconditioning on the cerebral transcriptional response to transient global cerebral ischemia. Methods Preconditioned and nonpreconditioned rats were exposed to 15 min of global cerebral ischemia, and changes in cerebral gene expression were identified by complementary DNA expression array and quantified by real-time reverse-transcription polymerase chain reaction. Results Ischemia caused a widespread up-regulation of transcription in nonpreconditioned brains in this model. Tolerance induction by erythromycin preconditioning reversed this pattern and caused a net down-regulation of a majority of genes, effectively reprogramming the brain's response pattern to ischemia. The most striking change in transcriptional response found in preconditioned animals was an almost complete suppression of the otherwise profound induction of proinflammatory genes by global ischemia. In contrast, the same treatment had little effect on the expression of apoptosis-inducing genes after ischemia. Conclusions These findings present a new molecular correlate for the induction of ischemic tolerance achieved by erythromycin preconditioning and will further the understanding of this clinically important new regimen of preemptive neuroprotection.
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Meng, Wei, Xiaoying Wang, Minoru Asahi, Tsuneo Kano, Kazuko Asahi, Robert H. Ackerman i Eng H. Lo. "Effects of Tissue Type Plasminogen Activator in Embolic versus Mechanical Models of Focal Cerebral Ischemia in Rats". Journal of Cerebral Blood Flow & Metabolism 19, nr 12 (grudzień 1999): 1316–21. http://dx.doi.org/10.1097/00004647-199912000-00004.
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Tissue type plasminogen activator (tPA) can be effective therapy for embolic stroke by restoring cerebral perfusion. However, a recent experimental study showed that tPA increased infarct size in a mouse model of transient focal ischemia, suggesting a possible adverse effect of tPA on ischemic tissue per se. In this report, the effects of tPA in two rat models of cerebral ischemia were compared. In experiment 1, rats were subjected to focal ischemia via injection of autologous clots into the middle cerebral artery territory. Two hours after clot injection, rats were treated with 10 mg/kg tPA or normal saline. Perfusion-sensitive computed tomography scanning showed that tPA restored cerebral perfusion in this thromboembolic model. Treatment with tPA significantly reduced ischemic lesion volumes measured at 24 hours by >60%. In experiment 2, three groups of rats were subjected to focal ischemia via a mechanical approach in which a silicon-coated filament was used intraluminally to occlude the origin of the middle cerebral artery. In two groups, the filament was withdrawn after 2 hours to allow for reperfusion, and then rats were randomly treated with 10 mg/kg tPA or normal saline. In the third group, rats were not treated and the filament was not withdrawn so that permanent focal ischemia was present. In this experiment, tPA did not significantly alter lesion volumes after 2 hours of transient focal ischemia. In contrast, permanent ischemia significantly increased lesion volumes by 55% compared with transient ischemia. These results indicate that in these rat models of focal cerebral ischemia, tPA did not have detectable negative effects. Other potentially negative effects of tPA may be dependent on choice of animal species and model systems.
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Chen, Jun, Roger P. Simon, Tesuya Nagayama, Raymond Zhu, J. Eric Loeffert, Simon C. Watkins i Steven H. Graham. "Suppression of Endogenous bcl-2 Expression by Antisense Treatment Exacerbates Ischemic Neuronal Death". Journal of Cerebral Blood Flow & Metabolism 20, nr 7 (lipiec 2000): 1033–39. http://dx.doi.org/10.1097/00004647-200007000-00002.
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Previous studies have shown that overexpression of bcl-2 in transgenic mice or by viral vectors protects the brain against cerebral ischemia. However, it is not known whether bcl-2, which is endogenously expressed in response to ischemia, exerts a protective effect. To address this question, the authors blocked the endogenous expression of bcl-2 after ischemia using antisense oligodeoxynucleotides (ODN). Antisense, sense, scrambled ODN, or vehicles were infused in the lateral ventricle of the rat for 24 hours after 30 minutes of temporary middle cerebral artery occlusion. Twenty-four hours later the brains were removed and bcl-2 protein expression was assayed by Western blot. Antisense ODN, but not sense or scrambled ODN treatment, significantly inhibited bcl-2 protein expression after ischemia. Bcl-2 protein expression was also studied 24 hours after 60 minutes of temporary middle cerebral artery occlusion in vehicle and antisense ODN-treated rats. After 60 minutes of ischemia and vehicle treatment, bcl-2 was expressed in many neurons in the ventral cortical mantle and the medial striatum. After antisense ODN treatment there were few neurons in this region expressing bcl-2, instead most neurons TUNEL labeled. Treatment with the antisense ODN, but not sense ODN, increased infarction volume as determined by cresyl violet staining 72 hours after ischemia compared with vehicle controls. These results suggested that endogenously expressed bcl-2 promoted survival in ischemic neurons and was not simply an epiphenomenon in neurons already destined to live or die.
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Caraban, B. M., Aurelia Romila, L. T. Hangan i Mihaela Lungu. "Cerebral Vasospasm in Subarachnoid Hemorrhage Through Aneurysm Rupture - Clinical Considerations and Case Report". ARS Medica Tomitana 22, nr 4 (1.11.2016): 232–38. http://dx.doi.org/10.1515/arsm-2016-0040.
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Abstract Arterial aneurysm ruptures of the circle of Willis determine subarachnoid hemorrhage, which evolving due to the irritating effect of the blood in the subarachnoid space may lead to complications such as large arterial vasospasm in the origin of the large cerebral arteries, from the base of the brain. Cerebral vasospasm causes a downstream cerebral ischemia, that may lead to the establishment of an ischemic stroke which is life threatening. Early treatment against the vasospasm with calcium channels blockers should prevent occurrence of ischemia. However, the effectiveness of this treatment is not fully confirmed, fact that was mentioned even in the presentation of our case.
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Sharma, Shyam S., Shankar Munusamy, Meenakshisundaram Thiyagarajan i Chaman L. Kaul. "Neuroprotective effect of peroxynitrite decomposition catalyst and poly(adenosine diphosphate—ribose) polymerase inhibitor alone and in combination in rats with focal ischemia". Journal of Neurosurgery 101, nr 4 (październik 2004): 669–75. http://dx.doi.org/10.3171/jns.2004.101.4.0669.
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Object. The authors evaluated the neuroprotective effect of 5,10,15,20-tetrakis(N-methyl-4′-pyridyl)porphyrinatoiron(III) (FeTMPyP), a peroxynitrite decomposition catalyst, and 1,5-isoquinolinediol (ISO), a poly(adenosine diphosphate [ADP]-ribose) polymerase (PARP) inhibitor, alone and in combination in rats with focal cerebral ischemia induced by middle cerebral artery occlusion (MCAO). Methods. Male Sprague—Dawley rats were subjected to 2 hours of MCAO followed by 22 hours of reperfusion. Cerebral infarction and neurological deficits were estimated after ischemia. Intraperitoneal injections of FeTMPyP (1 and 2 mg/kg) and ISO (0.05 and 0.1 mg/kg) were administered alone or in combination in ischemic animals. The PARP activity in vehicle- and drug-treated groups was estimated using anti—poly(ADP-ribose) antibody in immunofluorescence and immunoblotting studies. Two hours of MCAO and 22 hours of reperfusion produced significant cerebral infarction and neurological deficits. Treatment with FeTMPyP (1 and 2 mg/kg) and ISO (0.05 and 0.1 mg/kg) produced a significant reduction in cerebral infarction and neurological deficits. Combination therapy (2 mg/kg FeTMPyP and 0.1 mg/kg ISO) enhanced the inhibition of ischemic volume (77.81 ± 0.86%) compared with monotherapies (FeTMPyP 54.07 ± 5.6% and ISO 53.06 ± 3.88%). Immunoblotting and immunofluorescence studies showed PARP activation after ischemia, which was reduced by drug treatment. Conclusions. Neuroprotection observed with FeTMPyP and ISO alone and in combination may be attributed to inhibition of the peroxynitrite—PARP cascade of cerebral ischemia/reperfusion injury.
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Fedin, A. I. "Diagnosis and treatment of chronic cerebral ischemia". Consilium Medicum 18, nr 2 (2016): 8–12. http://dx.doi.org/10.26442/2075-1753_2016.2.8-12.
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Zakharov, V. V., N. V. Vakhnina, A. G. Gogoleva i S. K. Mezhmidinova. "Diagnostics and treatment of chronic cerebral ischemia". Meditsinskiy sovet = Medical Council, nr 8 (16.07.2020): 36–45. http://dx.doi.org/10.21518/2079-701x-2020-8-36-45.
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5560 patients with the diagnosis “Other cerebral vascular diseases” per 100 000 of elderly population were registered in RF in 2017. Usually this is a code for chronic brain ischemia (CBI) – the most popular diagnosis in Russian neurological practice. However, diagnostic criteria of CBI are not well defined and need to be ascertained. Recent studies show that the most reliable clinical feature of CBI could be cognitive impairment. It is developed before other clinical signs and correlate with severity of vascular brain lesions. Typically, cognitive impairment is subcortical with prominent bradyphrenia, attentional, dysexecutive and visuospatial deficit and relative sparing of memory. However clinical diagnosis of CBI could be only hypothetical. Diagnosis should be verified by MRI or other visualization technic. Diagnosis is verified if neuroimaging revealed silent strokes, microbleeds and vascular leukoencephalopathy. The most important objective of chronic brain ischemia management is the control of basic vascular disease. Besides this, pathogenetic therapy should be performed to improve cerebral microcirculation, neuronal metabolism and to provide neuroprotection. There is positive data on dipyridamole usage in chronic brain ischemia. It has desagregative, vasotropic, antioxidative and antiinflammation properties. Dypiridamole treatment in CBI patients lead to decrease of neuropsychiatric symptoms and improvement of well-being.