Dissertations / Theses on the topic 'Ouabain'
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Cellnik, Torsten [Verfasser]. "Defunktionalisierung von Ouabain / Torsten Cellnik." Wuppertal : Universitätsbibliothek Wuppertal, 2019. http://d-nb.info/118842209X/34.
Full textMagnusson, Emma. "Ouabain Toxicity -Selectivity Towards Renal Cancer Cells." Thesis, KTH, Skolan för kemi, bioteknologi och hälsa (CBH), 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-278574.
Full textOuabain och andra kardiotoniska steroider är kända för att inhibera Na + ,K + -ATPas (NKA),membranpumpen som är ansvarig för den aktiva jontransporten av natrium och kalium ochjongradienten över plasmamembranet. De har påvisat en selektiv toxicitet mot vissatumörceller i jämförelse med primära humana celler, men det är dock inte förstått hurmekanismen bakom denna företeelse fungerar. I denna studien undersökte vi ouabainstoxicitet i njurcancerceller (A-498) och papillomavirustransformerade proximala tubuliceller(hPTC) för att identifiera effektens nyckelkomponenter. Vid exponering av ouabain undersökte vi cellviabiliteten och -densiteten genom MTT- ochkristallviolett-analyser, samt cellmigrering genom scratch-analys. Den cytotoxiska effektenstuderades också under olika pH-förhållanden samt glukos- och kaliumkoncentrationer.Dessutom undersöktes det om apoptos orsakar celldöd genom TUNEL-analys, och omouabain dödar njurcancerceller genom aktivering av den volymreglerade anjonkanalen(VRAC) via NKA. Vi fann minskning av cellernas livskraft vid exponering av ≥ 10 nM ouabain, men effektentycktes dock inte se ut att vara selektiv gentemot cancerceller, inte heller på grund av apoptosoch aktivering av VRAC. Den cytotoxiska effekten var större vid lägre pH, men oberoendeav mediets glukoskoncentrationen. Intressant nog motverkades också effekten vid förhöjdkoncentration av kaliumjoner, och ouabain hämmade selektivt cancercellerna att migrera.Således finns det en viss potential för ouabain att kunna fungera som ett anticancermedel motnjurcancer och att hämma metastasutveckling.
Harwood, Steven Michael. "Development and application of an immunoassay for ouabain and a study of the nature of endogenous ouabain-like compound." Thesis, Queen Mary, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325540.
Full textCarneiro, Luciana Teles. "Efeito modulador da ouabaína no sistema imunológico." Universidade Federal da Paraíba, 2011. http://tede.biblioteca.ufpb.br:8080/handle/tede/6866.
Full textCoordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Initially known as a cardiotonic steroid capable to inhibit the Na+/K+ATPase, ouabain was identified as an endogenous substance present in human plasma, produced by the adrenal, pituitary and hypothalamus and can interfere with various aspects of immune response. In this study, which aimed to study the modulating effect of ouabain on the immune system in vivo and in vitro using mouse models, we demonstrated that treatment for three consecutive days using 0,56 mg/kg ouabain was able to reduce cell migration induced by mitogen Concanavalian A (Con A) to the peritoneum, and this fact reflects a decrease in the number of polymorphonuclear leukocytes, mainly neutrophils. In this same model, ouabain was also able to increase the number of mononuclear leukocytes in the peritoneal cavity. Evaluating the effect of treatment on lymphocytes in peripheral organs, we found that, in lymphocytes from mesenteric lymph nodes, this substance induces a decrease of 20% of T CD3+ lymphocytes, concomitant with an increase in same percentage of B lymphocytes, without, however, modulating the proportion of CD4+ and CD8+ among themselves, as well as the number of regulatory T cells (CD4+/CD25+). In the thymus, the same treatment, does not affect the proportion of lymphocyte subpopulations studied. The analysis qualitative and quantitatively of peripheral blood leukocytes, biometrics and cellularity of spleen, thymus and lymph nodes showed no change in response to ouabain treatment. Comparative studies using treatment for one or two days, with the same dose of 0,56 mg/kg did not trigger modulation, in vivo, in populations of T lymphocytes, B lymphocytes and subpopulations of CD4+ and CD8+ cells in mesenteric lymph nodes. In addition, ouabain was able to inhibit mitochondrial activity of lymphocytes stimulated with Con A, using MTT assay.These findings indicate an immunomodulatory role of ouabain.
Inicialmente, conhecida como um esteróide cardiotônico e por sua propriedade de inibir a Na+/K+ATPase, a ouabaína foi identificada como uma substância endógena presente no plasma humano, produzida pela adrenal, hipófise e hipotálamo e capaz de interferir em vários aspectos da resposta imune. Neste trabalho, que teve como objetivo estudar o efeito modulador da ouabaína no sistema imunológico in vivo e in vitro por meio de modelos murinos, demonstrou-se que o tratamento por três dias consecutivos com ouabaína utilizando a dose de 0,56 mg/kg foi capaz de reduzir a migração celular induzida pelo mitógeno Concanavaliana A (Con A) para o peritôneo, sendo este fato reflexo da redução do número de leucócitos polimorfonucleares, principalmente, neutrófilos. Neste mesmo modelo, a ouabaína também foi capaz de aumentar o número de leucócitos mononucleares no lavado peritoneal. Avaliando-se o efeito desse tratamento no perfil linfocitário de órgãos periféricos, encontrou-se que, em linfócitos de linfonodos mesentéricos, esta substância induz a uma diminuição de 20% de linfócitos T CD3+, concomitante a um aumento de mesmo percentual de linfócitos B, sem, no entanto, modular a proporção de linfócitos TCD4+ e CD8+ entre si, bem como o número de células T regulatórias (CD4+CD25+). No timo, o mesmo tratamento com a ouabaína não interfere na proporção das subpopulações linfocitárias estudadas. As análises qualitativas e quantitativas de leucócitos do sangue periférico, da biometria e celularidade do baço, timo e linfonodos mesentéricos não apresentaram alteração em resposta ao tratamento com a ouabaína. Estudos comparativos utilizando tratamentos de um ou dois dias, com a mesma dose de 0,56 mg/Kg não desencadearam modulação, in vivo, nas populações de linfócitos T, linfócitos B e das subpopulações de linfócitos TCD4+ e CD8+ nos linfonodos mesentéricos. Adicionalmente, a ouabaína foi capaz de inibir a atividade mitocondrial de linfócitos estimulados com Con A, por meio do ensaio de MTT. Estes resultados indicam um papel imunomodulador da ouabaína.
Tennant, Brian Prichard. "Biosynthesis and physiological characteristics of endogenous ouabain-like substance." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272367.
Full textSemra, Yemane Kurban. "Endogenous ouabain-like immunoreactive substance (OLIS) : characterisation and physiological studies." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313282.
Full textVasconcelos, Danielle Ingrid Bezerra de. "Análise do efeito imunomodulador da ouabaína na inflamação e nocicepção." Universidade Federal da Paraíba, 2011. http://tede.biblioteca.ufpb.br:8080/handle/tede/3640.
Full textCoordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Ouabain, known as a cardiotonic glycoside capable of inhibiting the Na+/K+ ATPase, was widely used for heart failure treatment. Identified as an endogenous substance, ouabain is capable of interfering with various physiological functions, including immune system modulation. Besides that, little is known about the involvement of this substance in nociceptive and inflammatory processes. The present study investigated the role of ouabain in acute peripheral inflammation induced by intraplantar administrartion of different phlogistic agents (carrageenan, compound 48/80, histamine, bradykinin, and PGE2) and in nociceptive processes (abdominal writhing induced by acetic acid and hot plate). Ouabain produced a significant reduction in the mouse paw edema induced by carrageenan and compound 48/80. This antiinflammatory effect of ouabain is associated to the inhibition of PGE2, bradykinin, and mast-cell degranulation, but not to histamine. Ouabain also presented a central and peripheral anti-nociceptive activity. This analgesic potential might be related to the inhibition of inflammatory mediators and to activation of opioid receptors, since it was reversed by naloxone, an opioid antagonist. Additionally, the analgesic effect of ouabain was not related to sedative effect or to motor function. Taken together, the present work demonstrated for the first time, in vivo, the antiinflammatory and analgesic potential of ouabain
A Ouabaína é um glicosídeo cardiotônico, inibidor da Na+/K+-ATPase, utilizada na clínica para o tratamento de insuficiência cardíaca. Atualmente, sabe-se que essa substância é endógena, e capaz de interferir em várias funções fisiológicas, inclusive em diversos aspectos do sistema imunológico. Apesar disso, pouco se sabe sobre seu envolvimento em processos inflamatórios e nociceptivos. Neste trabalho, foi avaliada a atividade da Ouabaína na inflamação aguda desencadeada pela administração de diversos agentes flogísticos (carragenina, composto 48/80, histamina, PGE2 e bradicinina) e em modelos nociceptivos (contorções abdominais induzidas por ácido acético e placa quente). A Ouabaína produziu uma redução no edema de pata produzido por carragenina e pelo composto 48/80. Esse potencial anti-inflamatório está relacionado ao bloqueio da degranulação de mastócitos, bem como pela inibição da via da PGE2 e da bradicinina, porém é independente da via da histamina. A Ouabaína também apresentou uma atividade anti-nociceptiva central e periférica. Esse efeito está vinculado à inibição da via dos mediadores inflamatórios e a mecanismos opióides, visto que foi revertido pela administração da naloxona, um inibidor dos receptores opióides. Adicionalmente, foi descrito que a inibição da dor pela Ouabaína não possui envolvimento com sedação ou diminuição da capacidade motora. O conjunto desses dados demonstra pela primeira vez, in vivo, a atividade anti-inflamatória e anti-nociceptiva da Ouabaína.
Gillingwater, Scott David. "Purification and characterisation of ouabain-like compound(s) from biological material." Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418070.
Full textHarris, Tanoya L. "Ouabain Regulates Caveolin-1 Vesicle Trafficking by a Src-Dependent Mechanism." University of Toledo Health Science Campus / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=mco1333732028.
Full textVeerasingham, Shereeni J. "Salt-induced hypertension, central regulation by ouabain-like compounds and angiotensin II." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ58297.pdf.
Full textFerguson, Alexandra Laura. "Studies on preconditioning with adenosine, glutamate and ouabain in rat hippocampal slices." Thesis, University of Glasgow, 2008. http://theses.gla.ac.uk/465/.
Full textYuan, Zhaokan. "Signaling Function of Na/K-ATPase in Ouabain-induced Regulation of Intracellular Calcium." University of Toledo Health Science Campus / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=mco1139325043.
Full textYeon, Kim. "Cardiotonic Steroids and the Sodium Potassium Pump." Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/25992.
Full textChawla, Rohit. "Vascular reactivity of isolated rat mesenteric arterioles in the presence and absence of ouabain." FIU Digital Commons, 2006. http://digitalcommons.fiu.edu/etd/2120.
Full textCai, Haiping. "Stimulation of apical NHE3 endocytosis by ouabain-activated basolateral Na/K-ATPase Signaling Complex." University of Toledo Health Science Campus / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=mco1209420160.
Full textWu, Jian. "Role of Phosphoinositide 3-Kinase a (PI3Ka) in Ouabain-induced Cardiac Signaling and Hypertrophy." University of Toledo Health Science Campus / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=mco1384283312.
Full textStebal, Cory J. "Isoform Specific Effect of Ischemia/Reperfusion on Cardiac Na,K-ATPase: Protection by Ouabain Preconditioning." University of Toledo Health Science Campus / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=mco1243946706.
Full textStebal, Cory. "Isoform specific effect of ischemia/reperfusion on cardiac Na,K-ATPase : protection by ouabain preconditioning." Connect to full text in OhioLINK ETD Center, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1243946706.
Full text"In partial fulfillment of the requirements for the degree of Master of Science in Biomedical Science." Title from title page of PDF document. Bibliography: p. 39-48.
Kinoshita, Paula Fernanda. "Sinalização inflamatória e a modulação da expressão de genes induzida pela ação da ouabaína nas isoformas a1, a2 - Na+, K+- ATPase em células da glia." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-24052014-103350/.
Full textNa,K-ATPase is a conserved membrane protein which maintains the osmotic balance in the cell by the hydrolysis of ATP. Ouabain (OUA) binds to Na,K-ATPase and it can activate signaling pathways. The a subunits of Na,K-ATPase have 4 isoforms which are distributed in a different pattern in the tissues. Glial cells have an important role in the response against injury and they also control inflammation. Some data have reported that OUA can protect against some types of injury. The aim of this study is to evaluate the role of a2 isoform in glial cells in response to OUA and LPS stimulus. We investigated the action of OUA and LPS in cell viability (LDH) and cell proliferation (MTT). LPS was used as a model of inflammation and one of our questions was if the treatment with OUA before LPS was capable of reduce the activation of the transcription factor NF-kB which is involved in inflammation. The pre-treatment with OUA decreased the NF-kB activation induced by LPS. We also silenced the a2 isoform in culture glial cells with iRNA. Taken together our data showed that OUA pretreatment reversed the NF-kB activation induced by LPS in primary cultures of glial cells from mice. Probably,the a2 isoform is related with some signaling pathway that interacts with the LPS pathway.
Hanke, Jana. "Can Ouabain Protect Transplantation Kidneys fromApoptosis?- Construction of an Experimental Set-Up to StudyStorage-Induced Apoptosis -." Thesis, KTH, Tillämpad fysik, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-147357.
Full textSaunders, Robert Peter. "Ouabain stimuliert Signalkaskaden und Zellproliferation in menschlichen Endothelzellen und erhöht die Expression und Freisetzung von Endothelin-1." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=974093629.
Full textKesiry, Riad. "GRP78/BiP is Involved in Ouabain-induced Endocytosis of the Na/K-ATPase in LLC-PK1 Cells." University of Toledo Health Science Campus / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=mco1096302498.
Full textLoreaux, Elizabeth L. "Role of the Ouabain-Binding Site of Na,K-ATPase in Saline Loading and DOCA-Salt Hypertension." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1213990314.
Full textTian, Jiang. "Na/K-ATPase, A Signaling Receptor." University of Toledo Health Science Campus / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=mco1175177603.
Full textHopoate-Sitake, Moana Lee. "A Novel Use of Digoxin Immune Fab Fragment in Identification and Isolation of an Endogenous Digitalis-like Factor Found in Preeclampsia." BYU ScholarsArchive, 2011. https://scholarsarchive.byu.edu/etd/2599.
Full textNeto, Hildebrando Candido Ferreira. "Papel dos rins na hipertensão arterial induzida pelo tratamento crônico com ouabaína em ratos." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-02022010-105527/.
Full textNa+K+-ATPase (NKA) is an integral membrane protein that participates in transport mechanisms along renal tubules for sodium reabsorption and other substrates. Its known that ouabain (OUA) administration, a NKA inhibitor, induces hypertension in Wistar rats. However, the role of kidneys in this model of hypertension is not elucidated. So, the aim of this study was to evaluate the possibles alterations in renal function induced by chronic treatment with OUA by 5 or 20 weeks. Chronic treatment with OUA induced hypertension in a similar magnitude in both experimental groups. Moreover, OUA administration was able to increase water intake, urinary flow, and protein expression of 1 isoform of NKA. However, OUA treatment did not alter significantly the glomerular filtration rate, likewise the fractional excretion of Na+ and K+. In summary, chronic OUA treatment induces mild hypertension independent of the period of administration, but the kidneys dont play an important role in the hypertensive process in this model of hypertension.
Pace, Iuri Domingues Della. "Efeito do Triterpeno 3β, 6β, 16β , trihidroxilup-20(29)-eno nas convul-sões induzidas por pentilenotretazol: papel da Na+, K+ ATPase." Universidade Federal de Santa Maria, 2013. http://repositorio.ufsm.br/handle/1/8993.
Full textEpilepsy is a syndrome characterized by spontaneous recurrent seizures, result of paroxys-mal discharges , excessive or synchronous a neural population . Despite the good prognosis, the high number of patients with epilepsy who have seizures refractory to medication, reflects the lack of a bet-ter understanding of excitotoxic disorders characteristic of this disease. Thus, it becomes important to understand the mechanisms for induction and maintenance of seizures as well, the search for new antiepileptic compounds that may prevent the development of this pathology. As nociception and epi-lepsy have mechanisms in common and several anticonvulsant drugs are used in treatment of pain , we investigated the effect of triterpene 3β , 6β , 16β Trihidroxilup -20 ( 29) -ene (TTHL), a compound with antinociceptive properties in convulsions induced by pentylenetetrazol (PTZ). The TTHL admin-istration ( 30 mg / kg , po) increased the latency to the first myoclonic seizures and tonic- clonic sei-zure and decreased the duration of generalized seizures induced by PTZ . In addition , the administra-tion of TTHL reduced lipid peroxidation and protein carbonylation , as well as protected from inhibition of glutamate uptake and activity of the Na+, K+-ATPase (α1and α2/α3 subunits ) caused by PTZ . Alt-hough the TTHL showed no antioxidant activity per se and not alter the binding of [ 3H ] flunitrazepam to the site of the GABAA receptor bezodiazepínico , this protected compound of convulsions and inhi-bition of Na+, K+-ATPase activity induced by ouabain . These results suggest that the anticonvulsant action is due TTHL s maintenance of Na+, K+-ATPase . In fact , the experiments performed in the cer-ebral cortex in vitro showed that PTZ ( 10 mM ) reduced the activity of Na+, K+-ATPase and that prein-cubation with TTHL ( 10 mM ) protected from this inhibition.Thus , these data indicate that the protec-tion exerted by TTHL this seizure model is not related to antioxidant activity or GABAergic activity . However, these results demonstrate that effective protection of Na+, K+-ATPase activity induced by this compound protects against oxidative and excitotoxic damage induced by PTZ .
A epilepsia é uma síndrome caracterizada por crises espontâneas e recorrentes, resultado de descargas paroxísticas, excessivas e sincrônicas de uma população neural. Apesar do bom prognós-tico, o elevado número de pacientes com epilepsia, que apresentam convulsões refratárias aos medi-camentos, reflete a falta de um melhor entendimento dos distúrbios excitotóxicos característico desta doença. Desta forma, torna-se importante o entendimento dos mecanismos de indução e manuten-ção das convulsões, bem como, a busca por novos compostos anticonvulsivantes que possam evitar o desenvolvimento desta patologia. Como a nocicepção e a epilepsia possuem mecanismos em co-mum, e vários anticonvulsivantes são usados no tratamento da dor, foi investigado o efeito do Triter-peno 3β,6β,16β Trihidroxilup-20(29)-eno (TTHL), um composto com propriedades antinociceptivas, nas convulsões induzidas pelo pentilenotetrazol (PTZ). A administração do TTHL (30 mg/kg; p.o) au-mentou a latência para a primeira convulsão mioclônica e tônico-clônica e reduziu a duração das convulsões generalizadas induzidas pelo PTZ. Além disso, a administração do TTHL reduziu a pero-xidação lipídica e a carbonilação de proteínas, assim como, protegeu da inibição da captação de glu-tamato e da atividade da Na+,K+-ATPase (subunidades α1 e α2/α3) causadas pelo PTZ. Embora, o TTHL não mostrou uma atividade antioxidante per se e não alterou a ligação do [3H]flunitrazepam ao sítio para bezodiazepínico do receptor GABAA, este composto protegeu das convulsões e da inibição da atividade da Na+, K+- ATPase induzidos pela ouabaina. Estes resultados sugerem que a ação an-ticonvulsivante do TTHL é devido s manutenção da atividade da Na+,K+-ATPase. De fato, os experi-mentos realizados no córtex cerebral in vitro mostraram que o PTZ (10 mM) reduziu a atividade da Na+,K+-ATPase e que a incubação prévia com TTHL (10 μM) protegeu desta inibição. Dessa forma, estes dados indicam que a proteção exercida pela TTHL neste modelo de convulsão não está relaci-onado com atividade antioxidante ou a atividade GABAérgica. No entanto, estes resultados demons-traram que a proteção eficaz da atividade da Na+,K+-ATPase , induzida por este composto, protege contra os danos excitotóxic e oxidativos induzidos pelo PTZ.
Tiruneh, Missale. "Angiotensin II Type 1 Receptor Activation in the Subfornical Organ Mediates Sodium-induced Pressor Responses In Wistar Rats." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23119.
Full textKalushkova, Antonia. "Epigenetic gene regulation in multiple myeloma and mood disorders." Doctoral thesis, Uppsala universitet, Hematologi och immunologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-199494.
Full textOrellana, Ana Maria Marques. "Administração intrahipocampal de Ouabaína ativa o NF - kB e a sinalização da proteína WNTem ratos." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-25052012-083840/.
Full textThe enzyme Na+,K+-ATPase is an integral membrane protein, highly conserved in eukaryotes, that establishes the electrochemical gradient across the plasma membrane, which is essential to maintain the osmotic balance of cells, the resting membrane potential and the excitatory property of nerve and muscle cells. Besides its role in ion homeostasis, several recent studies suggest that this pump may also act as a signal transducer and transcription activator involved in cell growth, differentiation and programmed cell death. Ouabain (OUA), the ligand of Na+,K+-ATPase, is a steroid derivative that is produced by the adrenal cortex and hypothalamus. After OUA binding, the Na+,K+-ATPase signaling seems to activate pathways such as Src, MAPK, NF-kB and Ca2+. Some evidences indicate a possible crosstalk between the NF-kB signaling pathway and the canonical WNT pathway, however the molecular mechanisms are still unknown. The canonical WNT play important roles during embryogenesis and in adult tissue homeostasis. The aim of this project is to verify if the intrahipocampal administration of OUA is able to modulate the activity of the canonical pathways of NF-kB and WNT. Both pathways were studied after 1 and 2 hours, and after 10, 24 and 48 hours by methods such Western blot, RT-PCR and Electrophoretic mobility shift assays. The results show that the OUA (10 nM) was able to activate the signaling pathway NF-kB after 1, 10, 24 and 48 hours. The OUA was also able to activate the canonical WNT pathway, since after 10 hours there was an increased in pGSK-3b protein, whereas in 24 hours, we observed increased nuclear translocation of b-CATENIN. Moreover, we found increased levels of BDNF throughout the time course.
Stricker, Joshua Lysle. "Protein Participants of Cytosolic Internalization of the Ouabain-bound Na+/K+ATPase Receptor in Human B-3 Lens Epithelial Cells." Wright State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=wright1524843508132212.
Full textKominato, Rieko. "Src activation generates reactive oxygen species and impairs metabolism-secretion coupling in diabetic Goto-Kakizaki and ouabain-treated rat pancreatic islets." Kyoto University, 2008. http://hdl.handle.net/2433/124247.
Full textWenceslau, Camilla Ferreira. "Papel da ouabaína endógena sobre o sistema cardiovascular do modelo de hipertensão arterial DOCA-SAL." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-18092012-085246/.
Full textIt has been shown that some types of hypertension have increased plasma levels of ouabain, a factor inhibitor of Na+K+-ATPase. In 1998, Ferrari et al. developed a molecule called rostafuroxin that antagonizes the effects of ouabain. In this context, it seems reasonable to suggest that an antihypertensive capable of antagonizing the effects of ouabain might be a new and specific pharmacological tool for the treatment of hypertension. In so doing, the present study aimed to evaluate the role of endogenous ouabain by treatment with rostafuroxin on blood pressure, vascular reactivity in resistance arteries and sympathetic activity of DOCA-salt rats. Our data have shown that the treatment with rostafuroxin decreased the systolic blood pressure and sympathetic activity and improve the vascular function of the DOCA-salt rats. Thus, it is suggested that ouabain is a putative target for the treatment of volume-dependent hypertension.
Wenceslau, Camilla Ferreira. "Efeito da administração crônica a longo prazo de ouabaína sobre a pressão arterial e a reatividade vascular de artérias mesentéricas de resistência de rato: possíveis mecanismos envolvidos." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-03062008-124025/.
Full textOuabain treatment (OUA) developed hypertension after 5, 10 and 20 weeks and modified the vascular function in mesenteric resistance arteries (MRA). 5-weeks treatment with OUA increased nitric oxide (NO) and neuronal isoform of nitric oxide (nNOS) protein expression. On the other side, this treatment reduced vasoconstrictors prostanoids. Besides decreased Cu-Zn superoxide dismutase (SOD) protein expression and increased functional activity of Na+K+-ATPase. 10-weeks treatment enhance NO and vasodilators prostanoids but reduced both nNOS and COX-2 protein expression. 20-weeks treatment reduced NO and nNOS protein expression. Nevertheless increased anion superoxide, tromboxan A2 and both SOD and COX-2 protein expression. In conclusion, OUA treatment induced HA and functional alterations in MRA that are time-dependents, because in 5 and 10 weeks of treatment these alterations are not likely to maintenance of HA, but the changes observed in the treatment during 20 weeks contributes.
Gabor, Alexander. "Role of Angiotensin II, Glutamate, Nitric Oxide and an Aldosterone-ouabain Pathway in the PVN in Salt-induced Pressor Responses in Rats." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22900.
Full textSilva, Juliane Santos de França da. "Efeito anti-inflamatório de ouabaína em modelo murino de lesão pulmonar aguda induzida por LPS." Universidade Federal da Paraíba, 2016. http://tede.biblioteca.ufpb.br:8080/handle/tede/9076.
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Ouabain is a cardiotonic steroid initially described as a substance of plant origin. In 1991, the endogenous production of higher mammals was identified and since then their physiological actions have been studied. Work of our group have demonstrated that ouabain modulates the acute inflammatory response induced by different phlogistic agents, also being able to interfere negatively in inflammatory profile triggered by Leishmania (L.) amazonensis. Acute lung injury (ALI) is a serious inflammatory disease characterized by acute inflammation, extensive accumulation of polymorphonuclear leukocytes and accumulation of proinflammatory mediators, which culminates with diffuse alveolar damage and which may cause the patient died due to severe hypoxemia. There is no data in the literature on the effects of ouabain in ALI. Objectives: Evaluate the immunomodulatory effect of ouabain in a murine model of ALI induced by LPS. Methods: BALB / c mice were treated intraperitoneally with ouabain at a dose of 0.56 mg / kg for a period of three consecutive days, 1 hour after the last treatment the animals were challenged intranasally with 40μl of an LPS solution (2 5 mg / kg); 24 hours after challenge, the animals were euthanized, the collected biological sample and inflammatory parameters, including cell migration, protein exudates, cytokine production, TLR4 expression and histopathological changes were then evaluated. Data were analyzed by PRISMA software. Results: The treatment with ouabain decreased total leukocytes migration to the inflamed site (48,84%), this event associated with decreased neutrophil migration (70,71%) and independent of macrophage migration. The ouabain also decreased the exudate protein in the broncho-alveolar region (26,32%) and production of the cytokines TNF-α (14,80%), IL-6 (47,07%) and IL1-β (33,59%), however this reduction in the production of these mediators was not related to the expression of TLR4. Additionally, the ALI histopathology changes were also reduced by treatment with ouabain. Conclusions: The results show that ouabain has anti-inflammatory action in ALI induced by LPS.
A Ouabaína é um esteroide cardiotônico inicialmente descrito como uma substância de origem vegetal. Em 1991, a sua produção endógena por mamíferos superiores foi identificada e desde então suas ações fisiológicas vêm sendo estudadas. Trabalhos do nosso grupo demonstraram que a ouabaína modula a resposta inflamatória aguda induzida por diferentes agentes flogísticos, sendo também capaz de interferir negativamente no perfil inflamatório desencadeado pela Leishmania (L.) amazonensis. A lesão pulmonar aguda (LPA) é uma doença inflamatória caracterizada por inflamação aguda e extenso acúmulo de polimorfonucleares e de mediadores pró-inflamatórios, que culmina com dano alveolar difuso podendo levar o paciente a óbito por hipoxemia severa. Não há dados na literatura sobre os efeitos da ouabaína na LPA. Objetivos: Avaliar o efeito imunomodulador de ouabaína em modelo murino de LPA induzida por LPS. Métodos: Camundongos BALB/c machos foram tratados via intraperitoneal com ouabaína na dose de 0,56 mg/Kg por um período de três dias consecutivos, 1h após o último tratamento os animais foram desafiados via intranasal com LPS (2,5 mg/Kg); 24h após o desafio, os animais foram eutanásiados, as amostras biológicas coletadas e os parâmetros inflamatórios, incluindo migração celular, exsudato proteico, produção de citocinas, expressão de TLR4 e alterações histopatológicas foram então avaliados. Os dados foram analisados pelo software PRISMA. Resultados: O tratamento com a ouabaína diminuiu a migração de leucócitos totais para o sítio inflamado (48,84%), evento este, associado a diminuição da migração de neutrófilos (70,7%) e independente da migração de macrófagos. Ouabaína também diminuiu o exsudato proteico na região bronco-alveolar (26,32%) e a produção das citocinas TNF-α (14,80%), IL-6 (47,07%) e IL1-β (33,59%), entretanto essa redução na produção desses mediadores não mostrou relação com a expressão do TLR4. Adicionalmente, as alterações histopatológicas características da LPA também foram reduzidas pelo tratamento com ouabaína. Conclusões: Os resultados obtidos demonstram que ouabaína possui ação anti-inflamatória na LPA induzida por LPS.
Banerjee, Moumita. "A Model for Domain-Specific Regulation of Src kinase by alpha-1 subunit of Na/K-ATPase." University of Toledo Health Science Campus / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=mco1385040354.
Full textBoström, Caroline. "Investigation on Cell-Cell Junctions by Inhibition of Na,K-ATPase Activity." Thesis, KTH, Tillämpad fysik, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-298360.
Full textDetta examensarbete undersöker effekten på cell-cell junctions när Na,K-ATPas (NKA) inhiberas. Målet med rapporten är att få en förståelse för hur NKA aktiviteten reglerar cell-cell junction proteinerna. Proteinerna som undersöks är adherens junction proteinet ECadherin, och tight junction proteinerna Claudin7 och Occludin. NKA inhiberas genom att cellerna behandlas med den kardiotoniska steroiden Ouabain. Behandlingen testas under olika tidsperioder och för olika koncentrationer. Resultaten visar att alla proteiner är nedreglerade när de behandlas med höga koncentrationer (500 nM) av Ouabain. ECadherin blir uppreglerad när det behandlas med lägre koncentrationer (10 nM) av Ouabain medan Claudin7 nedregleras vid låga nivåer.
Uhlén, Per. "Signal transduction via ion fluxes : a cell imaging study with emphasis on calcium oscillations /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-188-8.
Full textNguyen, Khoa Thuy Diem. "Energy metabolism in the brain and rapid distribution of glutamate transporter GLAST in astrocytes." Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/3996.
Full textNguyen, Khoa Thuy Diem. "Energy metabolism in the brain and rapid distribution of glutamate transporter GLAST in astrocytes." University of Sydney, 2008. http://hdl.handle.net/2123/3996.
Full textGlutamate transporters play a role in removing extracellular excitatory neurotransmitter, L-glutamate into the cells. The rate of the uptake depends on the density of the transporters at the membrane. Some studies claimed that glutamate transporters could transit between the cytoplasm and the membrane on a time-scale of minutes. The present study examined the distribution of glutamate transporter GLAST predominantly expressed in rat cortical cultured astrocytes between the membrane and the cytoplasm by using deconvolution microscopy and then analyzing the images. The regulation of the distribution of GLAST was studied in the presence of glutamate transporter substrate (D-aspartate), purinergic receptor activators (α,β-methylene ATP, adenosine), neuroleptic drugs (clozapine, haloperidol), ammonia (hyperammonia) and Na+/K+-ATPase inhibitors (ouabain, digoxin and FCCP). It was demonstrated that the translocation of GLAST towards the plasma membrane was induced by D-aspartate, α,β-methylene ATP, adenosine, clozapine and ammonia (at 100 μM and very high concentrations of 10 mM). However, the inhibition of Na+/K+-ATPase activity had an opposite effect, resulting in redistribution of GLAST away from the membrane. It has previously been claimed that the membrane-cytoplasm trafficking of GLAST was regulated by phosphorylation catalysed by protein kinase C delta (PKC-delta). Involvement of this mechanism has, however, been put to doubt when rottlerin, a PKC-delta inhibitor, used to test the hypothesis showed to inhibit Na+/K+-ATPase-mediated uptake of Rb+, suggesting that rottlerin influenced the activity of Na+/K+-ATPase. As Na+/K+-ATPase converts ATP to energy and pumps Na+, K+ ions, thus helping to maintain normal electrochemical and ionic gradients across the cell membrane. Its inhibition also reduced D-aspartate transport and could impact on the cytoplasm-to-membrane traffic of GLAST molecules. Furthermore, rottlerin decreased the activity of Na+/K+-ATPase by acting as a mitochondrial inhibitor. The present study has focused on the inhibition of Na+/K+-ATPase activity by rottlerin, ouabain and digoxin in homogenates prepared from rat kidney and cultured astrocytes. The activity of Na+/K+-ATPase was measured by the absorption of inorganic phosphate product generated from the hydrolysis of ATP and the fluorescent transition of the dye RH421 induced by the movement of Na+/K+-ATPase. This approach has a potential to test whether the rottlerin effect on Na+/K+-ATPase is a direct inhibition of the enzyme activity. Rottlerin has been found to block the activity of Na+/K+-ATPase in a dose-dependent manner in both rat kidney and astrocyte homogenates. Therefore, rottlerin inhibited the activity of Na+/K+-ATPase directly in a cell-free preparation, thus strongly indicating that the effect was direct on the enzyme. In parallel experiments, ouabain and digoxin produced similar inhibitions of Na+/K+-ATPase activity in rat kidney while digoxin blocked the activity of Na+/K+-ATPase to a greater extent than ouabain in rat cortical cultured astrocytes. In a separate set of experiments, Na+/K+-ATPase in the astrocytic membrane was found to be unsaturated in E1(Na+)3 conformation in the presence of Na+ ions and this could explain the differences between the effects of digoxin and ouabain on the activity of Na+/K+-ATPase in rat astrocytes. In addition, it was found that at low concentrations of rottlerin, the activity of Na+/K+-ATPase was increased rather than inhibited. This effect was further investigated by studying rottlerin interactions with membrane lipids. The activity of Na+/K+-ATPase has been reported to be regulated by membrane lipids. The enzyme activity can be enhanced by increasing fluidity of the lipid membrane. I have, therefore, proposed that rottlerin binds to the membrane lipids and the effects of rottlerin on Na+/K+-ATPase are mediated by changes in the properties (fluidity) of the membrane. The hypothesis was tested by comparing rottlerin and a detergent, DOC (sodium deoxycholate), for their binding to the lipids by using a DMPC (1,2-Dimyristoyl-sn-Glycero-3-Phosphocholine) monolayer technique. DOC has been shown to both increase and inhibit activity of Na+/K+-ATPase in a manner similar to that displayed by rottlerin. The effects of rottlerin and DOC on the DMPC monolayers were studied by measuring the surface pressure of DMPC monolayers and surface area per DMPC molecule. I established that both rottlerin and DOC decreased the surface pressure of DMPC monolayers and increased the surface area per DMPC molecule. This indicates that both rottlerin and DOC penetrated into the DMPC monolayers. If rottlerin can interact with the lipids, changes in fluidity of the lipid membrane cannot be ruled out and should be considered as a possible factor contributing to the effects of rottlerin on the activity of Na+/K+-ATPase. Overall, the study demonstrates that rottlerin is not only a PKC-delta inhibitor but can have additional effects, both on the enzyme activities (Na+/K+-ATPase) and/or on lipid-containing biological structures such as membranes. The findings have implication not only for studies where rottlerin was used as a supposedly specific PKC-delta inhibitor but also for mechanisms of its toxicity.
Batrel, Charlène. "Nouvelle méthode d'exploration fonctionnelle du nerf auditif." Thesis, Montpellier 1, 2014. http://www.theses.fr/2014MON13520/document.
Full textBackground: The synchronous activation of the auditory nerve fibers (ANFs), is commonly studied through the compound action potential (CAP), or the auditory brainstem responses (ABR), to probe deafness in experimental and clinical settings. Recent studies have shown that substantial ANF loss can coexist with normal hearing threshold, and even unchanged CAP amplitude, making the detection of auditory neuropathies difficult. In this study, we took advantage of the round window neural noise (RWNN) to probe ANF loss in a physiologically-relevant model of neuropathy.Material and methods: ANF loss was induced by the application of ouabain onto the round window niche. CAP and RWNN of the gerbil's cochlea were recorded through an electrode placed onto the round window niche, 6 days after the ouabain application. Afferent synapse counts and single-unit recordings were carried-out to determine the degree and the nature of ANF loss, respectively. Results: Application of a low ouabain-dose into the gerbil RW niche elicits a specific degeneration of low spontaneous rate (SR) fibers, as shown by single-unit recordings. Simultaneous recordings (CAP/single-unit) demonstrate that low-SR fibers have a weak contribution to the CAP amplitude because of their delayed and broad first spike latency distribution. However, the RWNN amplitude decreases with the degree of synaptic loss. The RWNN method is therefore more sensitive than CAP to detect low-SR fiber loss, most probably because it reflects the sustained discharge rate of ANFs. Based on these data, we proposed a far-field method (Peri-stimulus time response-PSTR) to assess the fast, slow, and sustain vesicular release at the first auditory synapse.Conclusion: The round window neural noise is a faithful proxy to probe the degree and the SR-based nature of fiber loss. This method could be translated into the clinic to probe hidden hearing loss and orient the practitioner toward synaptopathy and/or neuropathy.Key words: Cochlea, auditory nerve, compound action potential, round window neural noise, single fiber recording, ouabain-induced neuropathy
Lal, Mark. "Oxidative stress and calcium signalling : implications for diabetes and cardiac glycosides /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-583-2/.
Full textLi, Juan. "Na, K-ATPase as a signaling transducer /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-453-2/.
Full textRindler, Tara N. "Physiological Role of the α2-Isoform of the Na, K-ATPase in the Regulation of Cardiovascular Function." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1353343442.
Full textTang, Yong. "Impact de la perte des neurones cochléaires sur la fonction auditive." Thesis, Montpellier 1, 2011. http://www.theses.fr/2011MON1T022/document.
Full textDeafness is one of the most frequent sensory deficits in our industrialized societies. Among the auditory pathologies, sensorineural deafness is the most wide-spread. Sensorineural deafness is due to a dysfunction of the cochlea involving the ionic homeostasis, loss of sensory cells and spiral ganglion neurons. While an alteration of the homeostasis or the loss of sensory cells induce inevitably the appearance of deafness, the impact of spiral ganglion neuron loss is unknown.The object of this thesis was to estimate the impact of spiral ganglion neuron losses on the auditory function. We developed a pharmacological tool capable of creating a selective loss of spiral ganglion neurons, without damaging the presynaptic structures such as the sensory cells and the stria vascularis. To do this, we applied increasing doses of ouabain to the round window membrane in the gerbil. Electrophysiological evaluations such as the distortion product otoacoustic emissions, the endocochlear potential and the compound action potentials of the cochlear nerve were recorded before and 6 days after application of ouabain. At the end of the functional evaluations, the cochlea were removed and prepared for morphological evaluations using confocal microscopy and transmission electron microscopy.Our results showed that up to a concentration of 80 µM, ouabain did not induce any significant change of the amplitude of the distortion product otoacoustic emissions, which indicated a normal functional state of the outer hair cells, nor of the endocochlear potential which reflected an intact stria vascularis. On the other hand, the same concentrations of ouabain led to a dose-dependent decrease of the amplitude of the compound action potentials, which was strictly associated with a loss of spiral ganglion neurons and afferent synapses, as assessed by morpho-anatomical analyses. If the amplitude of the compound action potentials constitutes a good indicator of the number and the functional state of the spiral ganglion neurons and the afferent synapses, it is not the case for the audiometric thresholds. Indeed, a loss of 75 % of afferent synapses and more than 55 % loss of the ganglion neurons was necessary before an elevation of the audiometric thresholds was observed in the cochleae perfused with 80 µM ouabain. At 100 µM ouabain, the elevation of the auditory thresholds may result from the accumulated loss of sensory cells, damage to the stria vascularis, in addition to the loss of the spiral ganglion neurons and afferent synapses. All these results indicate that the application of ouabain onto the round window membrane in the gerbil is an excellent model to study the impact of the selective loss of the spiral ganglion neurons on hearing function. More generally, this study points towards the necessity of developing more precise tools, beyond the simple audiogram, for the investigation of auditory neuron loss in humans
Weitkamp, Christine. "Warum zeigen die Herzglykoside Ouabain und Digoxin unterschiedliche Kreislaufwirkung? Charakterisierung eines mutmasslichen Herzglykosid-Bindungsproteins im Serum und Analyse der Wirkung beider Steroide auf die Endothelin-1- und NO-Freisetzung aus arteriellen Endothelzellen /." Wettenberg : VVB Laufersweiler, 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=976405792.
Full textDuan, Qiming. "Cardiac Na/K-ATPase in Ischemia-Reperfusion Injury and Cardioprotection." University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1388151402.
Full textHao, Jingping. "The electrical properties of Bufo marinus Na⁺, K⁺-ATPase." Ohio : Ohio University, 2009. http://www.ohiolink.edu/etd/view.cgi?ohiou1258151062.
Full textTheriault, Steven F. "A role for the brain sodium, potassium-ATPase alpha2 isoform in salt-sensitive hypertension: Enhanced pressor responses to increased CSF sodium and ouabain concentrations in gene-targeted heterozygous alpha2 sodium, potassium-ATPase knockout mice." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/27058.
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