{"title":"Ischemic stroke models in adult experimental animals","authors":"A. Coşar","doi":"10.37212/jcnos.584699","DOIUrl":null,"url":null,"abstract":"Hypoxic-ischemia is containing complex physiological, molecular and biochemical pathways and it is induced by lack of oxygen supply to the brain. Hypoxic ischemia induces severe brain injury in adults and newborns. Pathophysiology of ischemic stroke involves oxidative stress, mitochondrial energy production failure, excessive Ca2+ influx and apoptosis (Akpinar, et al., 2016). Investigation of the traumatic brain injuries in the subject are difficult due to ethical restrictions. Therefore, the animal models have great importance for the clarifying etiology of the ischemic stroke-induced brain injuries. However, there are differences between human rodent brains. Notable difference between the human and rodent is presence of developing brain (Gennaro et al. 2019). In experimental animals, the best model of induction of hypoxic cerebral ischemic stroke is occlusion of the middle cerebral artery for 30-60 min (Gennaro et al. 2019). In addition to the best model, there are also other models of hypoxic cerebral stroke in rodents such as hypoxiaischemia, thrombotic ischemia, vasoconstriction. Endothelin 1 and the distal artery compression models (Gennaro et al. 2019; Hermann et al. 2019). In this presentation, I summarized the models currently used to investigate the human developmental ischemic stroke, describing their advantages and limitations.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cellular Neuroscience and Oxidative Stress","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.37212/jcnos.584699","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
引用次数: 0
Abstract
Hypoxic-ischemia is containing complex physiological, molecular and biochemical pathways and it is induced by lack of oxygen supply to the brain. Hypoxic ischemia induces severe brain injury in adults and newborns. Pathophysiology of ischemic stroke involves oxidative stress, mitochondrial energy production failure, excessive Ca2+ influx and apoptosis (Akpinar, et al., 2016). Investigation of the traumatic brain injuries in the subject are difficult due to ethical restrictions. Therefore, the animal models have great importance for the clarifying etiology of the ischemic stroke-induced brain injuries. However, there are differences between human rodent brains. Notable difference between the human and rodent is presence of developing brain (Gennaro et al. 2019). In experimental animals, the best model of induction of hypoxic cerebral ischemic stroke is occlusion of the middle cerebral artery for 30-60 min (Gennaro et al. 2019). In addition to the best model, there are also other models of hypoxic cerebral stroke in rodents such as hypoxiaischemia, thrombotic ischemia, vasoconstriction. Endothelin 1 and the distal artery compression models (Gennaro et al. 2019; Hermann et al. 2019). In this presentation, I summarized the models currently used to investigate the human developmental ischemic stroke, describing their advantages and limitations.
缺氧缺血是由大脑缺氧引起的复杂的生理、分子和生化途径。缺氧缺血可引起成人和新生儿严重脑损伤。缺血性卒中的病理生理涉及氧化应激、线粒体能量生产失败、过量Ca2+内流和细胞凋亡(Akpinar等,2016)。由于伦理的限制,对该学科的外伤性脑损伤的调查是困难的。因此,动物模型的建立对阐明缺血性脑损伤的病因具有重要意义。然而,人类啮齿动物的大脑是不同的。人类和啮齿动物之间的显著差异是存在发育中的大脑(Gennaro et al. 2019)。在实验动物中,诱导缺氧缺血性脑卒中的最佳模型是大脑中动脉闭塞30-60 min (Gennaro et al. 2019)。除最佳模型外,啮齿动物缺氧脑卒中还有缺氧缺血、血栓性缺血、血管收缩等模型。内皮素1与远端动脉压迫模型(Gennaro et al. 2019;Hermann et al. 2019)。在这篇报告中,我总结了目前用于研究人类发展性缺血性中风的模型,描述了它们的优点和局限性。
期刊介绍:
Journal of Cellular Neuroscience and Oxidative Stress isan online journal that publishes original research articles, reviews and short reviews on themolecular basisofbiophysical,physiological and pharmacological processes thatregulate cellular function, and the control or alteration of these processesby theaction of receptors, neurotransmitters, second messengers, cation, anions,drugsor disease. Areas of particular interest are four topics. They are; 1. Ion Channels (Na+-K+Channels, Cl– channels, Ca2+channels, ADP-Ribose and metabolism of NAD+,Patch-Clamp applications) 2. Oxidative Stress (Antioxidant vitamins, antioxidant enzymes, metabolism of nitric oxide, oxidative stress, biophysics, biochemistry and physiology of free oxygen radicals) 3. Interaction Between Oxidative Stress and Ion Channels in Neuroscience (Effects of the oxidative stress on the activation of the voltage sensitive cation channels, effect of ADP-Ribose and NAD+ on activation of the cation channels which are sensitive to voltage, effect of the oxidative stress on activation of the TRP channels in neurodegenerative diseases such Parkinson’s and Alzheimer’s diseases) 4. Gene and Oxidative Stress (Gene abnormalities. Interaction between gene and free radicals. Gene anomalies and iron. Role of radiation and cancer on gene polymorphism)