Dissertations / Theses on the topic 'Cerebral ischemia'
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Keasey, Matthew P. "MicroRNAs in Cerebral Ischemia." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526014.
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Molnar, Maria. "Hyperglycemia in Experimental Cerebral Ischemia." Doctoral thesis, Uppsala universitet, Anestesiologi och intensivvård, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-247763.
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Cerebral ischemia is a life-threatening condition associated with a substantial morbidity and mortality. Hyperglycemia, a common coexisting phenomenon in both stroke and cardiac arrest (CA), may further aggravate ischemic brain injury. To date, the therapeutic possibilities are lim-ited and the search for new treatment modalities is warranted. One aspect of such a research could be to better understand the cerebral pathogenesis induced by hyperglycemic ischemia-reperfusion. We investigated the combination of ischemia and hyperglycemia in two experimental models of stroke and CA. The aims were to test the neuroprotective potential of the sulfonated nitrone 2-sulfophenyl-N-tert-butylnitrone (S-PBN) in focal hyperglycemic cerebral ischemia (1), to outline the short-terms effects of hyperglycemia in prolonged (2) and short CA (3) and to performed a global transcriptome analysis of brain from hyperglycemic and normoglycemic CA (4). In a stroke model rats were made hyperglycemic prior to transient middle cerebral artery oc-clusion and randomized to S-PBN or saline. We found that S-PBN may ameliorate hyperglyce-mic-ischemic brain damage by improving the neurological performance after 1 day of survival, but did not reduce the infarct size. To study the cerebral oxidative state and perfusion after CA, pigs were randomized and clamped at blood glucose levels of 8.5 ̶ 10.0 mmol/L (high) and 4.0 ̶ 5.5 mmol/L (normal), sub-jected to 12 ̶ min of CA, followed by 8 min of cardiopulmonary resuscitation (CPR), and ob-served for 180 min. Increased oxygenation was found at higher glucose levels measured by near-infrared light spec-troscopy after CA. Tendencies toward increased protein S100β and 15-keto-dihydro-prostaglandin F2α were observed in the hyperglycemic group. We hypothesized that in combination with a brief period of CA, the preischemic hyperglycemia would worsen the cerebral injury compared with normoglycemia. We used a glycemic protocol similar to that in Paper II, whereby pigs were subjected to 5 ̶ min of CA, followed by 8 min of CPR, and observed for 180 mins. An increased level of the cerebral marker S100β was found in hyperglycemic pigs compared with normoglycemic pigs after CA. Global transcriptome analysis using microarray analysis revealed a different early metabolic gene expression in hyperglycemic CA compared with normoglycemic CA.
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Christensen, Thomas. "Experimental focal cerebral ischemia : pathophysiology, metabolism and pharmacology of the ischemic penumbra /." Copenhagen, 2007. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=016143698&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.
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Thorén, Anna. "Astrocyte metabolism following focal cerebral ischemia /." Göteborg : Institute of Neuroscience and Physiology, The Sahlgrenska Academy, Göteborg University, 2006. http://hdl.handle.net/2077/744.
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Thomas, Sunu Samuel. "Murine models of cerebral ischemia, development of a mouse model of global cerebral ischemia; response of GluR2 knockout mice in a model of permanent focal cerebral ischemia." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0026/MQ50439.pdf.
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Li, Yan. "Inhibitory synpatic transmission in striatal neurons after transient cerebral ischemia." Connect to resource online, 2009. http://hdl.handle.net/1805/2021.
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Thesis (Ph.D.)--Indiana University, 2009.Title from screen (viewed on December 1, 2009). Department of Anatomy and Cell Biology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Zao C. Xu, Feng C. Zhou, Charles R. Yang, Theodore R. Cummins. Includes vitae. Includes bibliographical references (leaves 115-135).
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Karelina, Ekaterina. "MECHANISMS OF SOCIAL NEUROPROTECTION AFTER CEREBRAL ISCHEMIA." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1274922479.
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Adhami, Faisal. "Differential Adult and Neonatal Response to Cerebral Ischemia-Hypoxia." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1196054266.
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Edrissi, Hamidreza. "Blood Brain Barrier Dysfunction in Chronic Cerebral Ischemia." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32531.
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Cerebral small vessel pathology is now known to be associated with the development of cognitive impairment and mild motor impairments such as gait disturbance in a variety of neurodegenerative diseases. This dissertation explores the hypothesis that blood brain barrier dysfunction is an early event in cerebral ischemia and contributes to the development of cerebral small vessel disease (CSVD). A common rodent model of CSVD is permanent bilateral common carotid artery occlusion in the rat. This model was used to study several aspects of the progression of CSVD including the timecourse of blood brain barrier permeability changes following the onset of ischemia, gait disturbance, the expression of tight junction proteins and cytokine expression. It was determined that BBB permeability was elevated for 2 weeks following BCCAO and ischemic rats displayed lower gait velocity. There was no change in expression of TJ proteins. However, ischemic rats had higher levels of some proinflammatory cytokines and chemokines in brain tissue with no obvious changes in plasma levels.
The mechanisms underlying the increase in BBB permeability were studied in vitro using artificial barriers made of confluent rat brain microvascular endothelial cells. Cerebral ischemia has been reported to cause an increase in plasma toxicity, likely by elevating the numbers of circulating microparticles (MPs). MPs isolated from the plasma of ischemic rats were applied to artificial barriers where it was found that they act mainly as vectors of TNF-α signaling. MPs induce activation of caspase-3 and the Rho/Rho kinase pathways. It is concluded that most of the increase in barrier permeability is due to apoptosis and disassembly of actin cytoskeleton and disruption of adherens junctions IV
and not an increase in transcellular transport.
The effects of treatment with the type III phosphodiesterase inhibitor cilostazol on dye extravasation in the brain, glial activation, white matter damage and motor performance were evaluated. It was determined that cilostazol could improve the increased BBB permeability and gait disturbance and microglial activation in optic tract following BCCAO. Also, the effects of treatment with cilostazol on plasma toxicity in vivo (24h and 14d following BCCAO) and artificial barriers (in vitro) were assessed. It was found that cilostazol could reduce plasma toxicity at 24h and improve increased endothelial barrier permeability that is induced by MP treatment respectively.
In summary BBB dysfunction occurs in the rat model of chronic cerebral hypoperfusion with no differences in expression of TJ proteins. There is a mild motor disturbance in the form of lower gait velocity following BCCAO. Cytokines released in brain tissue may be associated with pathological consequences following BCCAO while there is no significant difference in plasma levels and circulating MPs may play a role in BBB dysfunction.
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Ng, Kit-ying. "Neuroprotective effects of adiponectin in focal cerebral ischemia." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634371.
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Bogart, Robert William. "The effect of stress on global cerebral ischemia." Connect to resource, 2008. http://hdl.handle.net/1811/32235.
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Ng, Kit-ying, and 吳潔瑩. "Neuroprotective effects of adiponectin in focal cerebral ischemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634371.
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Raghavan, Aparna. "Neuroprotective Potential of Withania Somnifera in Cerebral Ischemia." University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1416570371.
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Schatlo, Bawarjan [Verfasser]. "Cerebral ischemia in experimental subarachnoid hemorrhage / Bawarjan Schatlo." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2011. http://d-nb.info/1026265347/34.
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Xu, Xingshun. "Novel Protective Agents against Cerebral Ischemia/Reperfusion Injury." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etd/2054.
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Stroke is the third leading cause of death and disability in the United States. At present, intravenous administration of tissue plasminogen activator (t-PA) is the only thrombolytic therapy approved by the FDA for the treatment of acute ischemic stroke. There are no other effective treatments available so far. The discovery of new drugs and new treatments for stroke to reduce mortality and disability is an urgent medical research priority. In this study, the protective effects and mechanisms of two novel agents Gly14 humanin (HNG) and necrostatin-1 (Nec-1) were examined. HNG, a highly potent neuropeptide against amyloid toxicity, exhibited anti-apoptotic properties on cerebral ischemia injury. HNG reduced infarct volume after ischemia/reperfusion injury with pre-treatment or post-treatment (i.c.v. and i.p.) in a middle cerebral artery occlusion model in mice and decreased neurological deficits induced by ischemia. The protection of HNG was mediated by inhibiting ERK activation and activating PI3K/Akt pathway. Inhibition of the PI3K/Akt pathway blocked the protective effects of HNG. Nec-1 is a specific inhibitor of necroptosis, a newly identified cell death, and was reported to reduce infarct volume even when it was administered at 6 h post-ischemia in a mouse stroke model. Interestingly, this small molecule protected against glutamate-induced oxidative toxicity in a hippocampal HT-22 cell line. It inhibited the translocation of apoptosis-inducing factor from the mitochondria to the nucleus, increased the cellular glutathione level, and decreased free radical formation after glutamate treatment. More importantly, Nec-1 inhibited BNIP3-mediated caspase-independent cell death. Cerebral ischemia/reperfusion injury involves the activation of different pathways that lead to neuronal cell death. Given this multifactorial pathnogenesis, it is possible that a cocktail of neuroprotective agents would be superior to monotherapy. In this study, a cocktail of HNG and Nec-1 was examined in vitro and in vivo. HNG and Nec-1 exerted synergistic neuroprotection on oxygen-glucose deprivation-induced cell death and cerebral ischemia/reperfusion injury. This study provided a new therapeutic strategy for the treatment of stroke by the combination of anti-apoptosis and anti-necroptosis therapy.
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Dowden, Jennifer. "Characterizing the neuroprotective efficacy of ischemic preconditioning (ischemic tolerance) : is age an important factor? /." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0019/NQ54834.pdf.
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Wang, Yanxin. "Hypoxic-ischemic injury in the neonatal rat model prediction of irreversible infarction size by Diffusion Weighted MR Imaging /." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B35757577.
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Frykholm, Peter. "Cerebral ischemia studied with positron emission tomography and microdialysis." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2002. http://publications.uu.se/theses/91-554-5319-8/.
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Slack, Penelope Jean. "Dietary n-3 fatty acids and cerebral ischemia/reperfusion." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/3992.
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Many populations have low intakes of n-3 fatty acids, yet there is substantial evidence that the long chain n-3 fatty acid docosahexaenoic acid (DHA; 22:6n-3), found at high concentrations in the brain, is required for the proper development of the nervous system. However, less is known about requirements of long chain n-3 fatty acids for maintenance and function of the nervous system in later life. Several recent studies have reported that high amounts of long chain n-3 fatty acids reduce the extent of brain damage caused by cerebral ischemia in animals. However, whether or not a dietary deficiency of n-3 fatty acids increases the extent of injury when cerebral ischemia occurs has not been previously reported. The present studies, therefore, sought to determine if a diet deficient in n-3 fatty acids influences the extent of brain injury in the rat following cerebral ischemia. Male rats were fed an n-3 fatty acid adequate (control), an n-3 fatty acid deficient, or a high DHA diet for 5 weeks from weaning. Middle cerebral artery occlusion (MCAO) was induced and infarct volume was measured by 2,3,5,-triphenyltetrazolium chloride staining 24 hours after the procedure. Brain and platelet fatty acids were analyzed by gas liquid chromatography. DHA (22:6n-3) was 21-28% lower in brain phospholipids, and 17% lower in brain total fatty acids in the n-3 fatty acid deficient compared to control group, while 22:6n-3 was 12% higher in total brain fatty acids in the high DHA group than the control group. There was no significant difference in infarct volume (203, 220 and 218 mm³) among the control, n-3 fatty acid deficient, and high DHA groups, respectively. Platelet fatty acids and platelet aggregation were assessed to determine if these were influenced by the high DHA diet, and could possibly explain the observation of an apparent, but not statistically significant, higher number of rats with hemorrhages in the high DHA diet group. Platelet lipid arachidonic acid was not lower and platelet aggregation, assessed ex vivo using whole blood with a platelet function analyzer, was not longer in rats fed the high DHA compared to control or n-3 fatty acid deficient diets. In summary, dietary n-3 fatty acid deficiency did not increase the extent of brain injury following cerebral ischemia. The possibility that high dietary 22:6n-3 might increase susceptibility to cerebral hemorrhage will require further study.
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Chaparro-Buitrago, Rafael Eduardo. "Neuroprotection with Anesthetics in Two Models of Cerebral Ischemia." Scholar Commons, 2010. http://scholarcommons.usf.edu/etd/3521.
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Neuroprotection with anesthetics has been studied for many decades; important advances in this field have modified the way Anesthesiologists treat patients in the operating room. Animal models have played an important role in the study of ischemia in the operating room. Recent studies have demonstrated that the effect of anesthetics seems to be different in different animal models. We decided to evaluate anesthetics in a well-known model of cerebral ischemia and also in hypotensive models designed by us. We used a model of cerebral ischemia (MCAO) to test anesthetics neuroprotective effect in a two-week period. Then, we used a model of hypotension to characterize the damage caused by this type of insult. Finally we characterized a model of hypotension plus hypoxia that can mimic real situations in the OR.
We found that anesthetics alone do not have a neuroprotective effect after two weeks in the MCAO model; but the combination of anesthetics with caspase inhibitors can decrease the damage caused by ischemia. The caspase inhibitor by itself did not show a significant neuroprotective effect.
We also found that repetitive periods of profound hypotension can cause important damage in the hippocampus but no memory or neurological changes were seen. The induction of only one episode of hypotension plus hypoxia did not alter the morphology of the hippocampus although induced memory changes that were reverted by the use of anesthetics.
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Schweizer, Sophie [Verfasser]. "Histone methylation and neuroprotection in cerebral ischemia / Sophie Schweizer." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2015. http://d-nb.info/1076270808/34.
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Blazej, Katja [Verfasser]. "Role of inflammatory cells in cerebral ischemia / Katja Blazej." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1031097007/34.
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Ward, Nicholas M. "The assessment of behavioural deficits following focal cerebral ischemia." Thesis, University of St Andrews, 1997. http://hdl.handle.net/10023/14698.
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Evaluating the efficacy of neuroprotective drugs in rat models of focal cerebral ischemia has involved histological and behavioural batteries to examine pathology and sensorimotor function. However, the behavioural tests used provide little insight into the nature of the neurological impairments. In an effort to gain further insight into the behavioural impairment following ischemic lesions, a battery of tasks were used. The tasks included tests of sensorimotor, motor (paw use), motivation, sensory and attentional function. The use of the potent vasoconstrictor endothelin-1 has allowed cerebral arteries to be occluded. This can be used to occlude the MCA (which is a common target of ischemia research), as well as other arteries, such as the ACA. Typically quantitative volumetric analysis has used nissl stains to assess lesion extent. However, alternative markers of tissue dysfunction are available including GFAP to assess the astroglial response to ischemia. Consequently cresyl violet and GFAP were compared along with different methods for calculating lesion volume. The boundaries of the lesion identified using the two stains corresponded closely providing care was taken when calculating lesion volume to avoid distortion from histological procedures and edema. Following MCA occlusion the rats displayed unilateral somatosensory and motor deficits, however there was no evidence of attentional dysfunction. Performance in the covert orienting task was compared with striatal dopamine depletion and with a posterior parietal cortical lesion. Neither of these manipulations resulted in deficits of covert orienting. Furthermore, the behavioural consequences of ACA occlusion were studied in two experiments using reaction time tasks designed to dissociate response impairments from dysfunction of motivation and attention. The ACA ischemic damage did not disrupt motivation or attention, however, the results were consistent with an impairment in selecting and initiating responses.
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Chan, Chu-fung. "Neuroprotective effects of granulocyte-colony stimulating factor in a mice stroke model." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B40687284.
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Gisselsson, Lars. "Ischemic brain damage the influence of hyperglycemia on tissue injury, cerebral circulation and edema formation /." Lund : Lund University, 1998. http://books.google.com/books?id=gMdrAAAAMAAJ.
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Li, Ping-An. "Mechanisms of acidosis-mediated ischemic brain damage histopathology and pathophysiology /." Lund : Lund University, 1996. http://catalog.hathitrust.org/api/volumes/oclc/38158955.html.
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Pereira, Claudia Figueiredo. "Carbon monoxide, autophagy and cytoprotection in response to cerebral ischemia." Master's thesis, Faculdade de Ciências e Tecnologia, 2013. http://hdl.handle.net/10362/10836.
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Dissertação para obtenção do Grau de Mestre em Genética Molecular e BiomedicinaThere is an increasing need for promoting neuroprotection against cerebral ischemia, which is the main cause of brain damage in adults. Astrocytes are the most abundant cells inboard the central nervous system (CNS), being known as key glial cell for promoting neuronal survival and homeostasis. It is more established in nowdays that astrocytic dysfunction contributes to neurodegenerative processes. Although, carbon monoxide is a well renown as a lethal and toxic gas due to its high affinity to hemoglobin, CO exerts anti-apoptotic, anti-inflammatory and anti-proliferative functions. Recent studies showed likewise that CO induces autophagy, promoting therefore cytoprotective and anti-inflammatory effects. Autophagy is a major catabolic pathway, known as an autodigestive process that degrades cellular organelles and proteins, playing an important role in cellular homeostasis during environmental stress. Due to the great interest on the signaling and cytoprotective actions of CO, novel strategies have been put forward to exploit the potential therapeutic effects of this gaseous molecule. One of these approaches consist on the development of CO-releasing molecules (CO-RMs), compounds that deliver small quantities of CO to tissues and first identified by the group of Motterlini and co-workers. The aim of this Master thesis was to study the action of CORM-A1, a boron-containing compound that spontaneously releases CO, against cell death in primary culture of astrocytes. In particular, we examined the role of CORM-A1 in autophagy, mitophagy and cell metabolism. Here, we demonstrated that CORM-A1 promotes the induction of autophagy in primary culture of astrocytes. Furthermore,autophagy is directly involved in the cytoprotective effect of CORM-A1 against cell death. In some preliminary experiments we have shown that CORM-A1 also induced mitophagy, while autophagy and inhibition of cell death promoted by CORM-A1 seem to occur under hypoxia (5% of oxygen). This master thesis has addressed several important questions on the role of CO in astrocyte function but also opened to many other important questions on the mechanism of action of CO. For instance, future work must be undertaken in order to explore whether CO-mediated induction of reactive oxygen species (ROS), which play an important role in cell signaling, which are the factors directly involved in mitophagy and the cross-talk between apoptosis and modulation of autophagy.
e-COST,(COST Action BM1005)
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BATTISTELLO, ENRICA. "PEMFs and cerebral ischemia: the pathways behind their beneficial effects." Doctoral thesis, Università degli studi di Ferrara, 2021. http://hdl.handle.net/11392/2488048.
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Low‐energy low‐frequency pulsed electromagnetic fields (PEMFs) exert numerous beneficial effects on different biological systems. In particular, several data have reported their neuroprotective role in cerebral ischemia, a disease that is a leading cause of mortality and disability worldwide.
For these reasons, PEMFs treatment has been introduced in a clinical multicentre, prospective, randomized, placebo‐controlled, and double‐blind study, whose aim is to investigate the effectiveness of PEMFs in acute ischemic stroke, as non-invasive and safe tool to gain neuronal recovery.
However, to date, little is known about the pathways used by PEMFs to mediate their positive outcome.
On these bases, the aim of this work was to investigate the molecular mechanism involved in PEMFs protective effects to contrast the hypoxic neuronal death and to decrease the neuroinflammation caused by microglial cells.
In particular, the first chapter of the thesis investigated the effects of PEMFs exposure on nerve growth factor‐differentiated pheochromocytoma PC12 cells, injured with hypoxia, and the pathway triggered by PEMFs to exert their effect. In detail, the fact that PEMFs mediated a protective effect on neuronal cell death in hypoxic condition was confirmed. For the first time, the neuroprotection was shown to depend on the rapid activation of p38 MAPK, enrolling HSP70 survival chaperone molecule, leading to an increase of pCREB, BDNF and finally modulating the antiapoptotic pathway regulated by the Bcl‐2 family of proteins.
The second chapter investigated the effects of PEMFs on microglial cells, key elements in modulating the neuroinflammation that follows the ischemic stroke. In particular, in lipopolysaccharide-treated N9 microglial cells, the cytokines production and the pathway involved were investigated, in the presence and in the absence of PEMFs. PEMFs inhibited the production of TNF-α and IL-1β induced by LPS, through the phosphorylation of JNK, and the secretion of IL-6, without affecting cells proliferation and viability. Interestingly, the pathway stimulated by PEMFs to reduce cytokines productions was different from the ones triggered by LPS to increase the pro-apoptotic mediators. In addition, it was proved that PEMFs can reduce crucial cell functions specific of activated microglia, like ROS generation, cell invasion and phagocytosis, which are essential to stop the inflammation.
To conclude, the results of this thesis showed that PEMFs manage to modulate different mediators in separate cell lines, producing distinct but beneficial effects in ischemic condition, suggesting PEMFs as a valid alternative therapeutic option for ischemic patients.I campi elettromagnetici pulsati a bassa energia e frequenza (PEMFs) stanno emergendo sempre più per i loro numerosi effetti benefici in molteplici sistemi biologici, sia in vitro che in vivo. Tra questi, diversi studi hanno dimostrato la capacità dei PEMFs di proteggere le cellule neuronali in seguito ad un evento ischemico. Questa patologia, riconosciuta a livello mondiale come una delle principali cause di morte e di disabilità permanente, non beneficia, ad oggi, di terapie o farmaci in grado di proteggere i neuroni, limitando il danno, e di favorire la ripresa del tessuto cerebrale colpito. In questo contesto si colloca il trattamento con i PEMFs. Infatti, grazie ai promettenti dati ottenuti, i PEMFs sono stati utilizzati in uno studio clinico multicentrico, prospettico, randomizzato, controllato con placebo e in doppio cieco, il cui scopo è indagarne l'efficacia nell'ictus ischemico acuto, al fine di impiegarli come strumento non invasivo e sicuro per il recupero neuronale. Sebbene, dunque, l’efficacia dei PEMFs sia riconosciuta, i pathways molecolari che innescano per mediare il loro effetto benefico sono ancora poco noti. Per questo motivo, lo scopo del mio lavoro di tesi è stato quello di investigare i mediatori attivati dai PEMFs sia nel contrastare la morte neuronale dovuta all’evento ipossico, sia nel diminuire la neuro-infiammazione a carico delle cellule microgliali. In particolare, nel primo capitolo della tesi sono stati investigati l’effetto dell’esposizione ai PEMFs sulle cellule neuronali PC12 (differenziate con il fattore di crescita neuronale NGF) sottoposte ad insulto ipossico, ed il pathway attivato dai campi elettromagnetici. Per la prima volta, i risultati ottenuti hanno mostrato un effetto protettivo dei PEMFs su queste cellule, diminuendone l’apoptosi provocata dall’ipossia. Il processo neuro-protettivo è stato scoperto essere mediato dal rapido coinvolgimento di p38 MAPK che a sua volta attiva HSP70, aumentando il livello di CREB fosforilato, reclutando BDNF e coinvolgendo infine il pathway anti-apoptotico regolato dalla famiglia di Bcl-2. Il secondo capitolo, invece, si è occupato degli effetti dei PEMFs sulle cellule microgliali che sono note per il loro ruolo fondamentale nella regolazione della neuro-infiammazione post-ischemia, e che sono coinvolte nel danno da riperfusione. Nel dettaglio, dunque, le cellule microgliali N9 sono state stimolate con un agente infiammatorio (il lipopolisaccaride, LPS) e sono stati investigati sia la produzione delle citochine pro-infiammatorie sia i relativi pathways coinvolti, con e senza il trattamento con i PEMFs. I risultati ottenuti hanno evidenziato l’abilità dei PEMFs di ridurre la secrezione di TNF-α e IL-1β tramite la modulazione di JNK, e di IL-6, senza alterare la vitalità e la proliferazione della microglia. Oltre alla produzione di citochine è stato ricercato anche l’effetto dei PEMFs nella regolazione di alcune funzioni specifiche delle cellule microgliali attivate, tra cui la produzione delle specie reattive dell’ossigeno, la fagocitosi e l’invasione cellulare. Nel dettaglio è stata riscontrata una riduzione di tutte in seguito al trattamento con i PEMFs, confermandone il ruolo essenziale nella diminuzione dello stato infiammatorio. I risultati di questo lavoro, dunque, hanno mostrato che il trattamento con i PEMFs è in grado di modulare numerosi mediatori sia nelle cellule neuronali che in quelle microgliali, contrastandone, rispettivamente, l’apoptosi e l’azione pro-infiammatoria, e per la prima volta, hanno descritto i meccanismi molecolari coinvolti. Questi risultati si aggiungono, dunque, a quelli pubblicati in altre linee cellulari, contribuendo a definire il meccanismo neuro-protettivo ed antinfiammatorio dei PEMFs e supportandone il loro utilizzo come terapia per l’ischemia cerebrale.
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Chen, Xiaoqian. "The identification of 14-3-3[gamma] in astrocytes and its mechanism in protecting astrocytes from ischemia /." View Abstract or Full-Text, 2002. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202002%20CHEN.
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Thesis (Ph. D.)--Hong Kong University of Science and Technology, 2002.Includes bibliographical references (leaves 180-202). Also available in electronic version. Access restricted to campus users.
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Mokhberi, Shiva. "ELECTRICAL BIOIMPEDANCE CEREBRAL MONITORING : A Study of Cerebral Impedance Variation." Thesis, KTH, Skolan för teknik och hälsa (STH), 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-190876.
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Stroke is amongst the leading causes of death and disability worldwide. Today diagnosis of Stroke is restricted to fixed imaging facilities which do not provide a rapid diagnostic. A portable device which could provide a non invasive assessment of stroke would therefore decrease the time of diagnosis and increase the chance of survival. Recent studies have confirmed that Implementing Electrical Bioimpedance in a portable device could provide a reliable means for Stroke diagnostic. However in order to be able to use the brain impedance as an indicator of Stroke, the invariance of brain impedance with time in healthy individuals should be studied first. Experimental Bioimpedance Spectroscopy (BIS) measurements from a healthy control group of 10 subjects have been used in this study to inspect the variation of brain impedance in the span of two weeks. The results of this study suggest that the cap which was used for brain impedance measurements together with the available device have not been an optimal way of measuring the brain impedance and therefore have affected the data by causing artifacts for the results. With the artifacts available in the data acquired in this study it is not possible to make any statements about the variation of brain impedance and therefore a deeper analysis of collected data using descriptive analysis is required in order to be able to judge on the significance of the obtained errors. In the future a larger study group should be considered in order to increase the predictive power of the observations.Stroke är bland de ledande orsakerna till död och funktionshinder i hela världen.I dagsläget är diagnos av stroke begränsad till fasta bildenheter som inte möjliggör en snabb diagnos. En bärbar enhet som möjliggör en icke invasiv bedömning av sjukdomen skulle minska diagnos tiden och följaktligen öka chansen att överleva sjukdomen. Genomförda studier i ämnet har bekräftat att implementering av Electrical Bioimpedance i en bärbar enhet kan räknas som ett effektivt sätt för Stroke diagnostik. För att kunna använda hjärnans impedans för Stroke diagnostik, bör först en studie av hjärnans impedans på friska individer utföras för att kunna visa att impedansen är oförändrad med tiden. Experimentell Bioimpedans Spektroskopi (BIS) mätningar från en frisk kontrollgrupp av 10 försökspersoner har utförts i denna studie för att inspektera variationen av hjärnans impedans under två veckor. Resultaten från denna studie tyder på att sättet av impedans mätningen i dagsläget är inte optimalt. Artefakter presenterad i resultatet gör det omöjligt för att kunna komma till ett beslut om hjärnans impedans variation . För fortsätta studier bör man överväga en större kontrollgrupp och även en analysering av data med hjälp av t-statistik som var inte inom ramen av denna studie.
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Silva, Matthew S. "NMR characterization of changes in the apparent diffusion coefficient of water following transient cerebral ischemia." Link to electronic thesis, 2002. http://www.wpi.edu/Pubs/ETD/Available/etd-0327102-221251.
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Tsang, Hing-wai, and 曾慶威. "In vitro studies of hypoxic ischemic down-regulated 1 (HID-1) protein encoded by a novel gene down-regulated in neonatal hypoxic-ischemicencephalopathy in different cell death paradigms." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45608192.
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Zou, Liangyu. "Role of cerebral ischemia in cognitive impairment clinical and experimental study /." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B32019889.
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Davis, Stephanie. "Leukemia Inhibitory Factor as a Neuroprotective Agent against Focal Cerebral Ischemia." Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6218.
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Previous publications from this laboratory demonstrated that administration of leukemia inhibitory factor (LIF) (125 µg/kg) to young, male Sprague-Dawley rats at 6, 24, and 48 h after middle cerebral artery occlusion (MCAO) reduced infract volume, improved sensimotor skills, and alleviated damage to white matter at 72 h after the injury. In vitro studies using cultured oligodendrocytes (OLs) showed that LIF (200 ng/ml) also protects against 24 h of oxygen-glucose deprivation through activation of Akt signaling and upregulation of the antioxidant enzymes peroxiredoxin IV and metallothionein III. Other groups have demonstrated that LIF reduces neurodegeneration in animal models of disease, but the neuroprotective mechanisms of LIF during permanent ischemia have not yet been examined. The overall hypothesis to be tested in this project is whether LIF exerts similar protective mechanisms against neurons during ischemia through increased antioxidant enzyme expression in neurons.
In the first set of experiments, superoxide dismutase (SOD) activity was significantly increased in the ipsilateral hemisphere of LIF-treated rats compared to rats that received PBS treatment at 72 h after MCAO. Western blot and immunohistochemical analysis revealed that SOD3 was upregulated in brain tissue and induced specifically in cortical neurons tissue at this time point. Neurons that expressed high levels of SOD3 at 72 h after MCAO also showed high levels of phosphorylated Akt (Ser473). LIF (200 ng/ml) reduced necrotic and apoptotic cell death against 24 h of OGD as measured by lactate dehydrogenase (LDH) release and caspase-3 activation. Quantitative real-time PCR analysis showed that LIF treatment upregulated SOD3 gene expression in vitro during OGD. Treatment with 10 µM Akt Inhibitor IV and transfection with SOD3 siRNA counteracted the neuroprotective effects of LIF in vitro, showing that upregulation of SOD3 and activation of Akt signaling are necessary for LIF-mediated neuroprotection.
Several transcription factors that regulated Akt-inducible genes were previously identified by this lab, including myeloid zinc finger-1 (MZF-1) and specificity protein-1 (Sp1). The goal of the second set of experiments was to determine whether LIF exerted protective actions through MZF-1 and Sp1. According to analysis with Genomatix, MZF-1 and Sp1 have multiple binding sites in the promoter for the rat SOD3 gene. Western blot analysis showed that there was a trend towards increased MZF-1 protein expression in the brains of LIF-treated rats that approached significance. Immunohistochemical analysis and quantitative real-time PCR showed a significant in vitro upregulation in MZF-1 expression among LIF-treated neurons compared to PBS-treated neurons. Sp1 gene expression was not changed by LIF treatment, but there was a trend towards increased protein expression. In addition, there was a significant correlation between Sp1 and MZF-1 among brain samples from LIF-treated rats but not PBS-treated or sham rats at 72 h after MCAO. Immunohistochemical analysis revealed that Sp1 and MZF-1 co-localized with neuronal nuclei and SOD3 at 72 h after MCAO. Neurons that were transfected with MZF-1 or Sp1 siRNA following isolation did not show a significant decrease in LDH release after 24 h OGD that was observed among neurons transfected with scrambled siRNA. These data demonstrate that Sp1 and MZF-1 are involved with the neuroprotective signaling of LIF under ischemia.
This laboratory has demonstrated that LIF activates transcription of protective genes and increases the activity of transcription factors through modulation of intracellular signaling. However, the upstream signaling mechanisms of LIF during ischemia had not previously been investigated. Previous investigators found that the LIF-specific subunit of the heterodimeric LIF receptor (LIFR) is induced by CNS injury. Western blot analysis was used to determine whether LIFR was induced in the brain and the spleen, which plays a role in the peripheral immune response, after MCAO. According to these results, LIF treatment significantly upregulates LIF in the brain compared to PBS treatment or sham injury at 72 h after MCAO. Genomatix analysis of the LIFR promoter region revealed a binding site for Sp1, which is one of the transcription factors responsible for neuroprotection by LIF. At this same time point, splenic LIFR expression is significantly reduced after MCAO compared to sham injury. LIF treatment did not significantly increase LIFR expression, but did significantly increase spleen size compared to PBS treatment at 72 h after MCAO. Although there was a trend towards increased LIFR expression in the spleen from 24 h to 72 h after MCAO, this increase was not statistically significant. However, there was a significant positive correlation between spleen weight and LIFR expression among rats euthanized 24-72 h after MCAO/sham injury. In addition, there was a significant negative correlation between LIFR expression in the brain and the spleen weight, thus showing that LIFR is upregulated following the splenic response.
According to findings from other groups, JAK1 has been shown to associate with the heterodimeric LIF receptor (LIFR/gp130) and directly activate PI3K/Akt signaling. To test whether JAK1 contributes neuroprotection during ischemia, cultured neurons were treated with several concentrations (2.5-50 nM) of GLPG0634, a JAK1-specific inhibitor prior to 24 h of OGD. With the exception of the 2.5 nM concentration, all concentrations of GLPG0634 significantly decreased LDH release compared to DMSO treatment, with the 5 nM concentration having the most potent effect on reducing cytotoxicity. However, the 5 nM concentration had no significant did not significantly reduce LDH release compared to DMSO treatment under 24 h of normoxic conditions. These results indicate that JAK1 activity is primarily detrimental to neurons during ischemia. Although it is possible that LIF signaling activates JAK1, it is unlikely that JAK1 is responsible for LIF-mediated neuroprotection during ischemia.
The results of these experiments allowed us to determine several molecular mechanisms for LIF-mediated neuroprotection. LIF, which binds to its heterodimeric receptor, activates Akt signaling during ischemia. The transcription factors Sp1 and MZF-1, which are located downstream of Akt, bind to the promoter of the SOD3 gene. In addition, Sp1 also regulates the LIFR gene. SOD3 upregulation increases total SOD activity, which decreases apoptotic and necrotic cell death during apoptosis. Due to its ability to promote antioxidant expression and survival signaling in multiple neural cell types, LIF shows promise as a novel treatment for permanent focal cerebral ischemia.
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Zou, Liangyu, and 鄒良玉. "Role of cerebral ischemia in cognitive impairment: clinical and experimental study." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B32019889.
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Vasylieva, N. V. "Chronic cerebral ischemia and cognitive impairment (an effect of complex therapy)." Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/17642.
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Gaudier-Diaz, Monica M. "Sex-Specific Social Modulation of the Neuroinflammatory Response toGlobal Cerebral Ischemia." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1490713683841079.
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Chan, Chu-fung, and 陳柱峰. "Neuroprotective effects of granulocyte-colony stimulating factor in a mice stroke model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B40687284.
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Pogoryelova, Oksana. "A study of epigenetics in ischaemic stroke." Thesis, University of Aberdeen, 2013. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=201969.
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Ischaemic stroke rates are expected to rise significantly in the next decades due to an aging population. This increases the demand for new stroke biomarkers for early detection of patients at risk and new targets for treatment. It has been hypothesized that epigenetics may be important in the aetiology of stroke. The study consisted of three types of investigation: analysis of candidate gene polymorphism, candidate gene methylation analysis and epigenome-wide methylation analysis (EWAS) of pooled stroke and control samples. The stroke types studied were large vessel disease (LVD), small vessel disease (SVD) and cardioembolic stroke (CE). DNA from peripheral blood samples was used for EWAS and methylation analysis. Significant increases in rare allele frequency were observed in the EHMT2 and DNMT3B genes for all stroke cases; MBD2, DNMT3B and DNMT3L polymorphisms were associated with LVD. IL10, SOD3, LINE1 and PITX2 were significantly hypomethylated in LVD. IL10 and ALOX15 were hypomethylated in CE compared to controls. Methylation levels of following genes were associated with age (LINE1, IL10, MTHFR, TNFα, and PITX2), gender (SOD3 and LINE1), total cholesterol level (SOD3) and systolic blood pressure (IL10). HDAC9 genetic polymorphism was associated with the MTHFR methylation level. A distinctive methylation pattern for each stroke subtype was found by EWAS. The CE pool was hypomethylated at genome, chromosome and gene level, while LVD and SVD pools had regions with higher and lower methylation levels compared to the controls. GNAS was identified as new candidate gene by EWAS. The results suggested that genetic polymorphism and DNA methylation levels of candidate genes were associated with ischaemic stroke. Stroke subtypes had distinct methylation profiles suggesting differences in underlying aetiology. Variations in methylation levels detected in this study could lead to identification of specific biomarkers. Replication on a large number of subjects is required before final conclusions can be drawn.
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Pennings, Frederik Anthonius. "The clinical value of assessing cerebral ischemia: emphasis on brain tissue oxygenation and function of the cerebral microcirculation." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2007. http://dare.uva.nl/document/45158.
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Sidhu, Ranjinder S. "Role of apoptosis following cerebral hypoxia-ischemia in immature and older rats." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0014/MQ32247.pdf.
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Kostulas, Nikolaos. "Studies on cytokines and chemokines in cerebrovascular diseases and experimental cerebral ischemia /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4701-5/.
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Zur, Nedden Stephanie. "Targeting the purine salvage pathway in in vitro models of cerebral ischemia." Thesis, University of Warwick, 2011. http://wrap.warwick.ac.uk/45926/.
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An interruption of the blood supply to the brain, as occurs during ischemic stroke, results in a rapid decline of ATP levels and a subsequent loss of neuronal function and viability. Under physiological conditions the brain reuses ATP degradation metabolites, such as hypoxanthine, via the purine salvage pathway, to restore its ATP pool. However, the massive degradation of ATP during ischemia results in the accumulation and loss of diffusible purine metabolites and thereby leads to a reduction in the post-ischemic ATP pool size, leaving the brain more vulnerable to secondary ischemic insults (recurrent strokes) and less able to deploy reparative mechanisms. The aim of this study was to improve the recovery of post-ischemic ATP levels by enhancing the purine salvage pathway, with substances that are already known to be tolerated in humans. Using acute hippocampal rat brain slices, I found that 1 mM Ribose (Rib) and 50 μM Adenine (Ade), two main metabolites of the purine salvage pathway, significantly increased the tissue ATP levels under basal conditions. Rib/Ade pre-treatment results in accelerated decline of synaptic transmission after onset of oxygen/glucose deprivation (OGD), due to increased adenosine release. However, this intervention does not delay the onset of anoxic depolarisation, or improve the recovery of synaptic transmission after prolonged ischemic periods. Pre-treatment of brain slices with 1 mM creatine, which increases phosphocreatine levels and thereby buffers the rapid decline of ATP levels upon energy shortage, significantly delays the onset of AD and helps to improve the recovery of synaptic transmission. By using cultured cerebellar granule cells, for more protracted studies on cell viability after OGD, I show that addition of Rib/Ade after ischemia helps to improves cell viability. Therefore my results suggest that both, delaying the decline of ATP upon onset of OGD (pre-treatment with creatine), or enhancing the post-ischemic recovery of ATP (post-treatment with Rib/Ade) are useful strategies to improve cell survival and function after in vitro ischemia.
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Xu, Mingjing, and 徐明婧. "Baicalin protects neural cells from cerebral ischemia reperfusion injury by scavenging peroxynitrite." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47753110.
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Ischemic stroke is the leading cause of death and disability in human diseases all around the world. As effective treatment for ischemic stroke is still absent, seeking for new therapy is of great interest. Currently, several key pathological cascades following cerebral ischemia have been explored to develop further therapies. Among them, reactive nitrogen species (RNS) has been indicated to play a critical role in cerebral ischemia reperfusion injury. As one of the RNS, peroxynitrite contributes to the neural cell death and subsequent brain dysfunction in the process. Thus, development of antioxidants targeting on peroxynitrite could be an important strategy for the treatment of cerebral ischemia-reperfusion injury.
Baicalin is a polyphenolic compound isolated from roots of Scutellaria baicalensis. Baicalin exerted protective effects against cerebral ischemia-reperfusion injury but the mechanisms are not clear yet. In this study, we investigated the free radical scavenging ability and neuroprotective effects of baicalin. According to our results, baicalin neutralized DPPH radicals effectively. By using electron paramagnetic resonance (EPR) spin trapping technology and fluorescent probe DAF-2DA, we found that baicalin dose-dependently scavenged superoxide, but had very low effect on elimination of nitric oxide. The immunofluoresent results revealed that baicalin at the concentration of 50 M completely suppressed the nitrotyrosine formation induced by 3-morpholinylsydnoneimine chloride (SIN-1, a peroxynitrite donor) in neuroblastoma SH-SY5Y cells. Mass spetrum provided direct evidence of the peroxynitrite scavenging ability of baicalin. Using MTT assays, we found that baicalin totally reversed peroxynitrite-induced cytotoxicity in SH-SY5Y cells and protected SH-SY5Y cells in oxygen glucose deprivation (OGD) and following reoxygenation injury. Furthermore, in vivo experiments revealed that intravenous injection of baicalin exerted better neuroprotective effect than intraperitoneal administration in rats underwent middle cerebral artery occlusion (MCAO). After cerebral ischemia reperfusion, rats treated with 3 mg/kg of peroxynitrite decomposition catalyst (FeTMPyP) or 25 mg/kg of baicalin revealed a smaller size of infarction volume, suppressed neural cell death and reduced nitrotyrosine formation than MCAO rats. However, baicalin did not alter the expression of tight junction proteins, claudin-5 and ZO-1, in brain endothelial bEnd3 cell line treated with OGD following reoxygenation. In cerebral ischemia reperfusion rats, administration of FeTMPyP at the dosage of 3 mg/kg diminished the Evans blue leakage caused by blood brain barrier disruption, whereas treatment of baicalin did not show significant effect.
In conclusion, this study suggests that baicalin can scavenge peroxynitrite and protect neural cells from peroxynitrite-induced injury. Furthermore, baicalin could prevent brains from cerebral ischemia-reperfusion injury and the neuroprotective mechanisms are associated with the scavenging effects on peroxynitrite. These findings provide new insights into the antioxidant and neuroprotective properties of baicalin and indicate the potential application of baicalin for the treatment of ischemic stroke.published_or_final_version
Chinese Medicine
Master
Master of Philosophy
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Syrett, Andrew J. "Bioactive Glycerophospholipids and Their Role in Modulating Neuronal Vulnerability Following Cerebral Ischemia." Thesis, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20536.
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Stroke is a devastating and debilitating condition resulting from a blockage or
hemorrhage in the vasculature of the brain. Despite extensive research, the etiology
and pathophysiology of the disease at the level of the cell membrane are poorly
understood, and effective treatment has been elusive. Though much research has
shown marked increases in lipid metabolism following stroke, the impact of these
changes have often been overlooked given the technical challenges associated with
identifying regionally specific changes in degenerating tissue. The advent of
lipidomics – a systems biology approach to the large-scale profiling of individual
lipid species in tissues – has renewed interest in understanding the role of
membrane lipids and their metabolites in the cell and in ischemic injury. In this
thesis, I have used an unbiased LC-ESI-MS-based lipidomic approach to profile the
small molecular weight glycerophosphocholine second messenger lipidome in
anterior and posterior regions of cortex and striatum in the forebrain of wild-type and
platelet activating factor receptor (PAFR) null-mutant mice before and after middle
cerebral artery occlusion (MCAO). From these profiles, I have outlined the potential
use of lipid second messenger distribution as topographic landmarks to identify
functional subdomains within neural tissue. Further, I have demonstrated that
ischemia does not simply disrupt lipid second messenger metabolism globally but
produces regionally specific changes in discrete species and that these changes are
altered by the loss of lipid regulatory effectors (i.e., PAFR null mutation). Based on
the lipid species identified in this profile of healthy and ischemic tissue, I proposed
that tight regulation of PC(O-22:6/2:0) homeostasis by PAFR-expressing microglia is
ii
required for proper dopaminergic signaling in prefrontal cortex. Finally, I have
outlined a model whereby increased PAF synthesis following ischemia contributes
the inflammatory response by promoting blood-brain barrier permeability, microglial
activation and immune cell infiltration in a PAFR-dependent manner.
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Cordell, Ryan [Verfasser]. "The relationship between the blood-brain barrier and cerebral ischemia / Ryan Cordell." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2012. http://d-nb.info/1028496222/34.
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Queiroga, Cláudia Susana Fernandes. "Disclosing Carbon Monoxide Protection in Cerebral Ischemia: Insights into the cellular mechanisms." Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica, 2012. http://hdl.handle.net/10362/10869.
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Dissertation presented to obtain the PhD degree in Biochemistry, NeurosciencesThe present work demonstrates the ability of carbon monoxide (CO) to prevent apoptosis in primary culture of astrocytes. For the first time, the anti-apoptotic behaviour can be clearly attributed to the inhibition of mitochondrial membrane permeabilisation (MMP), a key event in the intrinsic apoptotic pathway. In isolated non-synaptic mitochondria CO partially inhibits (i) loss of membrane potential, (ii) the opening of a non specific pore through the inner membrane, (iii) swelling and (iv) cytochrome c release, which are induced by calcium, diamide or atractyloside (a ligand of adenine nucleotide translocase, ANT). CO directly modulates ANT function by enhancing ADP/ATP exchange and prevents its pore-forming activity.(...)
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Padayachy, L. C. "The prevalence of cerebral hypoxia/ischemia in pediatric severe traumatic brain injury." Master's thesis, University of Cape Town, 2010. http://hdl.handle.net/11427/2887.
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Li, Han-Dong, Minshu Li, Elaine Shi, Wei-Na Jin, Kristofer Wood, Rayna Gonzales, and Qiang Liu. "A translocator protein 18 kDa agonist protects against cerebral ischemia/reperfusion injury." BIOMED CENTRAL LTD, 2017. http://hdl.handle.net/10150/625392.
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Background: Cerebral ischemia is a leading cause of death and disability with limited treatment options. Although inflammatory and immune responses participate in ischemic brain injury, the molecular regulators of neuroinflammation after ischemia remain to be defined. Translocator protein 18 kDa (TSPO) mainly localized to the mitochondrial outer membrane is predominantly expressed in glia within the central nervous system during inflammatory conditions. This study investigated the effect of a TSPO agonist, etifoxine, on neuroinflammation and brain injury after ischemia/reperfusion. Methods: We used a mouse model of middle cerebral artery occlusion (MCAO) to examine the therapeutic potential and mechanisms of neuroprotection by etifoxine. Results: TSPO was upregulated in Iba1(+) or CD11b(+) CD45(int) cells from mice subjected to MCAO and reperfusion. Etifoxine significantly attenuated neurodeficits and infarct volume after MCAO and reperfusion. The attenuation was pronounced in mice subjected to 30, 60, or 90 min MCAO. Etifoxine reduced production of pro-inflammatory factors in the ischemic brain. In addition, etifoxine treatment led to decreased expression of interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha, and inducible nitric oxide synthase by microglia. Notably, the benefit of etifoxine against brain infarction was ablated in mice depleted of microglia using a colony-stimulating factor 1 receptor inhibitor. Conclusions: These findings indicate that the TSPO agonist, etifoxine, reduces neuroinflammation and brain injury after ischemia/reperfusion. The therapeutic potential of targeting TSPO requires further investigations in ischemic stroke.
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Oyamada, Naofumi. "The Role of Mineralocorticoid Receptor Expression in Brain Remodeling after Cerebral Ischemia." Kyoto University, 2009. http://hdl.handle.net/2433/124289.
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