Pub Date : 2020-01-01DOI: 10.1016/b978-0-12-818606-0.00030-4
Hyewon Kong, N. Chandel
{"title":"Reactive oxygen species and cancer","authors":"Hyewon Kong, N. Chandel","doi":"10.1016/b978-0-12-818606-0.00030-4","DOIUrl":"https://doi.org/10.1016/b978-0-12-818606-0.00030-4","url":null,"abstract":"","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78229046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-01-01DOI: 10.1016/b978-0-12-818606-0.09995-8
{"title":"Copyright","authors":"","doi":"10.1016/b978-0-12-818606-0.09995-8","DOIUrl":"https://doi.org/10.1016/b978-0-12-818606-0.09995-8","url":null,"abstract":"","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75687766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-01-01DOI: 10.1016/b978-0-12-818606-0.00037-7
V. Miguel, S. Lamas
{"title":"Redox distress in organ fibrosis: The role of noncoding RNAs","authors":"V. Miguel, S. Lamas","doi":"10.1016/b978-0-12-818606-0.00037-7","DOIUrl":"https://doi.org/10.1016/b978-0-12-818606-0.00037-7","url":null,"abstract":"","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86552974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-01-01DOI: 10.1016/b978-0-12-818606-0.09988-0
{"title":"Index","authors":"","doi":"10.1016/b978-0-12-818606-0.09988-0","DOIUrl":"https://doi.org/10.1016/b978-0-12-818606-0.09988-0","url":null,"abstract":"","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89556787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The aim of this study was to determine cadmium neurotoxicity (Branca et al. 2018) and beneficial effect of quercetin (QE) (Kanter et al. 2016) against on neuronal damage in hippocampus exposed with acute cadmium (Cd). Adult male Wistar-Albino rats (n = 30) were used and divided into four groups as Control (C, n = 6), Cadmium (Cd, n = 8), Quercetin (Q, n = 8) and Cadmium + Quercetin (Cd + Q, n = 8). Cadmium (CdCl2, 4 mg kg-1 daily, s.c) were administrated to Cd and Cd+Q groups, and Quercetin (Q, 50 mg kg-1 daily, i.p) were administrated to Q and Cd + Q groups for 3 days, respectively. At 4th day after the treatments, hippocampal samples were taken from the four groups. Cadmium decreased superoxide dismutase (SOD) and reduced glutathione (GSH) levels and the SOD activity and GSH level were markedly (p< 0.05) lower in Cd group than in the Q and C groups. Lipid peroxidation (MDA) levels were higher in Cd group when compared to the control, Q and Cd+Q groups. IL1 levels were found statistically higher in Cd group than in the control, Q and Cd+Q groups. IL-6 and TNF-alfa levels were significantly (p< 0.05) higher in Cd and Cd+Q groups than the Q and C groups. In addition, IL10 levels were detected the lowest in Cd group when compared to other groups. In conclusion, our results show that quercetin can be beneficial against to neurotoxic effects of acute cadmium toxicity in the rat hippocampus through upregulation of antioxidant system but down regulation of cytokine levels.
本研究的目的是确定镉的神经毒性(Branca et al. 2018)和槲皮素(QE) (Kanter et al. 2016)对暴露于急性镉(Cd)的海马神经元损伤的有益作用。选用成年雄性wiast - albino大鼠30只，分为对照(C, n = 6)、镉(Cd, n = 8)、槲皮素(Q, n = 8)和镉+槲皮素(Cd +Q, n = 8) 4组，Cd组和Cd+Q组分别给予镉(CdCl2, 4 mg kg-1 / d, s.c)和槲皮素(Q, 50 mg kg-1 / d, i.p)，试验期为3 d。治疗后第4天，取各组海马标本。镉降低了超氧化物歧化酶(SOD)和谷胱甘肽(GSH)水平，且Cd组SOD活性和谷胱甘肽水平显著(p< 0.05)低于Q和C组。脂质过氧化(MDA)水平在Cd组高于对照组、Q组和Cd+Q组。Cd组il - 1水平明显高于对照组、Q组和Cd+Q组。Cd和Cd+Q组IL-6和tnf - α水平显著高于Q和C组(p< 0.05)。此外，与其他各组相比，Cd组检测到的IL10水平最低。综上所述，槲皮素可通过上调抗氧化系统而下调细胞因子水平来对抗急性镉中毒大鼠海马的神经毒性作用。
{"title":"The effects of quercetin on antioxidant and cytokine levels in rat hippocampus exposed to acute cadmium toxicity","authors":"I. Kisadere, N. Dönmez, H. H. Dönmez","doi":"10.37212/JCNOS.584684","DOIUrl":"https://doi.org/10.37212/JCNOS.584684","url":null,"abstract":"The aim of this study was to determine cadmium neurotoxicity (Branca et al. 2018) and beneficial effect of quercetin (QE) (Kanter et al. 2016) against on neuronal damage in hippocampus exposed with acute cadmium (Cd). Adult male Wistar-Albino rats (n = 30) were used and divided into four groups as Control (C, n = 6), Cadmium (Cd, n = 8), Quercetin (Q, n = 8) and Cadmium + Quercetin (Cd + Q, n = 8). Cadmium (CdCl2, 4 mg kg-1 daily, s.c) were administrated to Cd and Cd+Q groups, and Quercetin (Q, 50 mg kg-1 daily, i.p) were administrated to Q and Cd + Q groups for 3 days, respectively. At 4th day after the treatments, hippocampal samples were taken from the four groups. Cadmium decreased superoxide dismutase (SOD) and reduced glutathione (GSH) levels and the SOD activity and GSH level were markedly (p< 0.05) lower in Cd group than in the Q and C groups. Lipid peroxidation (MDA) levels were higher in Cd group when compared to the control, Q and Cd+Q groups. IL1 levels were found statistically higher in Cd group than in the control, Q and Cd+Q groups. IL-6 and TNF-alfa levels were significantly (p< 0.05) higher in Cd and Cd+Q groups than the Q and C groups. In addition, IL10 levels were detected the lowest in Cd group when compared to other groups. In conclusion, our results show that quercetin can be beneficial against to neurotoxic effects of acute cadmium toxicity in the rat hippocampus through upregulation of antioxidant system but down regulation of cytokine levels.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43548840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Atypical aggregation of α-synuclein in the brain is linked to Parkinson’s disease (PD) progression. Mutimers of α-synuclein may be important for the biological function of α-synuclein. Currently, reliable methods to compare α-synuclein multimer abundance in biological samples are limited and sophisticated. A new technique termed “multimer-PAGE,” was designed by Killinger and Moszczynska, which combines in-gel chemical cross-linking with several common electrophoretic techniques to measure the multimerization of α-synuclein in complex biological samples of brain tissue lysates. Using this technique, it was possible to compare the ratio of α-synuclein multimers between brain tissue samples without the need for specialized equipment.
{"title":"Aggregates of α-synuclein in brain tissue homogenates measured by newly designed Multimer-PAGE techniques","authors":"J. Saleh","doi":"10.37212/JCNOS.584670","DOIUrl":"https://doi.org/10.37212/JCNOS.584670","url":null,"abstract":"Atypical aggregation of α-synuclein in the brain is linked to Parkinson’s disease (PD) progression. Mutimers of α-synuclein may be important for the biological function of α-synuclein. Currently, reliable methods to compare α-synuclein multimer abundance in biological samples are limited and sophisticated. A new technique termed “multimer-PAGE,” was designed by Killinger and Moszczynska, which combines in-gel chemical cross-linking with several common electrophoretic techniques to measure the multimerization of α-synuclein in complex biological samples of brain tissue lysates. Using this technique, it was possible to compare the ratio of α-synuclein multimers between brain tissue samples without the need for specialized equipment.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44487473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mohammad A. I. Al-Hatamleh, Imilia Ismail, Omar Mahmoud Al-shajrawi, T. M. Ariff
The present study aimed to evaluate the effect of stress on haematological parameters among preclinical medical students. A cross-sectional study has been conducted on a total of 105 preclinical medical students at Faculty of Medicine, Universiti Sultan Zainal Abidin (UniSZA), Terengganu, Malaysia. The validated depression anxiety stress scales-21 (DASS-21) questionnaire was distributed and blood samples were collected from the subjects on the same day to perform full blood count (FBC) test. There was no significant association between levels of stress with red blood cells (RBCs) count and indices. However, a significant negative association was identified between stress level and white blood cells (WBCs) count (r= - 0.204, p ≤ 0.05). Furthermore, no significant association was found between levels of stress and platelets count and indices, except the mean platelets volume (MPV); a significant positive association between students measured MPV and their perceived stress (r= 0.195, p ≤ 0.05) has been noted. Mean WBCs count was decreased, while mean MPV was increased with increasing stress levels. Furthermore, the structural equation model predicted that some parameters were near to be significantly associated with stress, which needs further investigation. This study provided novel insights about the potential effects of stress on blood cells and platelets. The results will help the researchers to uncover the critical areas of increasing ROS and oxidative stress caused by chronic life stress.
{"title":"Effect of stress on alteration of haematological parameters: A preliminary study on preclinical medical students in Malaysia","authors":"Mohammad A. I. Al-Hatamleh, Imilia Ismail, Omar Mahmoud Al-shajrawi, T. M. Ariff","doi":"10.37212/jcnos.683403","DOIUrl":"https://doi.org/10.37212/jcnos.683403","url":null,"abstract":"The present study aimed to evaluate the effect of stress on haematological parameters among preclinical medical students. A cross-sectional study has been conducted on a total of 105 preclinical medical students at Faculty of Medicine, Universiti Sultan Zainal Abidin (UniSZA), Terengganu, Malaysia. The validated depression anxiety stress scales-21 (DASS-21) questionnaire was distributed and blood samples were collected from the subjects on the same day to perform full blood count (FBC) test. There was no significant association between levels of stress with red blood cells (RBCs) count and indices. However, a significant negative association was identified between stress level and white blood cells (WBCs) count (r= - 0.204, p ≤ 0.05). Furthermore, no significant association was found between levels of stress and platelets count and indices, except the mean platelets volume (MPV); a significant positive association between students measured MPV and their perceived stress (r= 0.195, p ≤ 0.05) has been noted. Mean WBCs count was decreased, while mean MPV was increased with increasing stress levels. Furthermore, the structural equation model predicted that some parameters were near to be significantly associated with stress, which needs further investigation. This study provided novel insights about the potential effects of stress on blood cells and platelets. The results will help the researchers to uncover the critical areas of increasing ROS and oxidative stress caused by chronic life stress.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45696638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Neurological disorders are an important cause of mortality and constitute 11.84% of total deaths globally according to WHO data 2015. It is estimated to increase up to 12.22% in year 2030. Most common NDs can be account for four main groups such as Alzheimer’s disease (AD), Amyotrophic Lateral Sclerosis (ALS), Huntington’s disease (HD) and Parkinson’s disease (PD). Among these diseases, only AD is the seventh common death cause worldwide and until recently the therapeutic approaches are still lack to decrease of prevalence. Hence, developing new strategies to understand molecular targets or break down to cascade of cellular degenerative process in the neurodegeneration should be investigated by future studies. In cell culture studies, many types of tissues and cells can be cultivated to be a minimized model to normal or pathophysiological status of disorders. There are lots of methodology or technique to compose efficient and respective neurodegenerative disease models in cell lines such as COS-7, HC2S2, HEK-293, HeLa, Neuro-2a, NSC-34, PC-12, and SH-SY5Y. We indicated best medium formula to growth of neuronal cells as well as differentiation chemicals and time/dosages. In the review it was aimed to summarize not only give information about cell lines, methodological procedures and molecular mechanisms of the diseases but also represent future perspective and offers to this field of neuroscience research.
{"title":"Experimental cell culture models for investigating neurodegenerative diseases","authors":"A. Öz","doi":"10.37212/JCNOS.683400","DOIUrl":"https://doi.org/10.37212/JCNOS.683400","url":null,"abstract":"Neurological disorders are an important cause of mortality and constitute 11.84% of total deaths globally according to WHO data 2015. It is estimated to increase up to 12.22% in year 2030. Most common NDs can be account for four main groups such as Alzheimer’s disease (AD), Amyotrophic Lateral Sclerosis (ALS), Huntington’s disease (HD) and Parkinson’s disease (PD). Among these diseases, only AD is the seventh common death cause worldwide and until recently the therapeutic approaches are still lack to decrease of prevalence. Hence, developing new strategies to understand molecular targets or break down to cascade of cellular degenerative process in the neurodegeneration should be investigated by future studies. In cell culture studies, many types of tissues and cells can be cultivated to be a minimized model to normal or pathophysiological status of disorders. There are lots of methodology or technique to compose efficient and respective neurodegenerative disease models in cell lines such as COS-7, HC2S2, HEK-293, HeLa, Neuro-2a, NSC-34, PC-12, and SH-SY5Y. We indicated best medium formula to growth of neuronal cells as well as differentiation chemicals and time/dosages. In the review it was aimed to summarize not only give information about cell lines, methodological procedures and molecular mechanisms of the diseases but also represent future perspective and offers to this field of neuroscience research.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45247539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Microglia are immune cells colonized in the central nervous system (CNS) during the development of the embryo. They make up about 12% of the glial cell population in the brain. These cells play an important role in eliminating the damage that may occur in the CNS or in carrying out normal functions. Microglia cells, which are in morphologically inactive form, are characterized by small cell body, small amounts of cytoplasm and cellular extensions that are released towards the environment. They undergo a significant morphological change and switch to the active form in a pathophysiological condition in the CNS, and they have the ability to migrate to the damaged area by ameboid movement. In today's studies, microglial cells in the active form has been stated to show neuroprotective and neurotoxic effects in neuronal structures in addition to carrying out phagocytosis of metabolic residues in the medium. It has also been mentioned in recent studies that microglial cells located in the CNS have a highly sensitive activation mechanism against inflammation and pathological conditions. Understanding the microglial activation mechanism in neurodegenerative diseases is thought to may contribute to the diagnosis / treatment of neurological diseases as well as being a diagnostic marker for the etiology of the diseases. In this review, the general characteristics and activation mechanism of microglial cells and their functional roles in Alzheimer's, Parkinson's, epilepsy and multiple sclerosis diseases were discussed in the current review.
{"title":"Microglia and its role in neurodegenerative diseases","authors":"Kenan Yıldızhan, M. Nazıroğlu","doi":"10.37212/jcnos.683407","DOIUrl":"https://doi.org/10.37212/jcnos.683407","url":null,"abstract":"Microglia are immune cells colonized in the central nervous system (CNS) during the development of the embryo. They make up about 12% of the glial cell population in the brain. These cells play an important role in eliminating the damage that may occur in the CNS or in carrying out normal functions. Microglia cells, which are in morphologically inactive form, are characterized by small cell body, small amounts of cytoplasm and cellular extensions that are released towards the environment. They undergo a significant morphological change and switch to the active form in a pathophysiological condition in the CNS, and they have the ability to migrate to the damaged area by ameboid movement. In today's studies, microglial cells in the active form has been stated to show neuroprotective and neurotoxic effects in neuronal structures in addition to carrying out phagocytosis of metabolic residues in the medium. It has also been mentioned in recent studies that microglial cells located in the CNS have a highly sensitive activation mechanism against inflammation and pathological conditions. Understanding the microglial activation mechanism in neurodegenerative diseases is thought to may contribute to the diagnosis / treatment of neurological diseases as well as being a diagnostic marker for the etiology of the diseases. In this review, the general characteristics and activation mechanism of microglial cells and their functional roles in Alzheimer's, Parkinson's, epilepsy and multiple sclerosis diseases were discussed in the current review.","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44385537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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。
{"title":"Ischemic stroke models in adult experimental animals","authors":"A. Coşar","doi":"10.37212/jcnos.584699","DOIUrl":"https://doi.org/10.37212/jcnos.584699","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":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48862879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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