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Id: lil-676173
Autor: Cornejo, R; Matamala, F; Silva, H; Garrido, O; Jaramillo, R; Sáez, L; Painemil, S; Loncoñanco, E.
Título: Efecto de estimulaciones infrarrojas sobre hepatoesteatosis microvesicular alcohólica de ratas / Infrared laser effect on alcoholic rat hepatic microvesicular steatosis
Fonte: Int. j. morphol;31(1):307-311, mar. 2013. ilus.
Idioma: es.
Projeto: DIUFRO.
Resumo: 24 ratas hembras de 4 meses de vida con peso aproximado de 250 gramos fueron divididas en dos grupos de animales, A y B. Ambos grupos se mantuvieron con pellet y solución de alcohol 40% durante 60 días generándoseles una hepatoesteatosis microvesicular. Los hígados de los animales pertenecientes al grupo B fueron estimulados con láser infrarrojo 6 J/cm2 durante 15 días consecutivos. Posteriormente, las ratas fueron sacrificadas y se extrajeron muestras de hígado y luego procesadas para microscopía electrónica de transmisión. De ambos tipos celulares se obtuvieron microfotografías electrónicas de transmisión con aumentos finales de 8.500 X, las cuales fueron sometidas a estudios morfométricos para determinar fracciones volumétricas de los siguientes componentes celulares: Retículo endoplasmático rugoso (RER), mitocondrias, inclusiones lipídicas y de glicógeno, eu y heterocromatina. De igual manera se cuantificaron las áreas celulares y nucleares. Del análisis de los resultados entre hepatocitos esteatósicos e irradiados se visualiza que existen diferencias en todos los componentes celulares cuantificados y se concluye que los efectos de la estimulación infrarroja con dosis de 6 J/cm2 provoca en los hepatocitos con esteatosis microvesicular transformación en su ultraestructura y en su morfología, fundamentalmente en la disminución acentuada de las infiltraciones lipídicas hasta en un 80% situación que se traduciría, en una variación funcional, representando de esta manera un efecto evidente que estas inducciones infrarrojas generan.

24 four-month-old female rats weighing approximately 250 grams were divided into two groups labeled A and B. Both groups were fed pellets and a 40% alcohol solution for 60 days, which caused a microvesicular hepatic steatosis. The livers of the animals in Group B were stimulated with 6 J/cm2 of infrared laser for 15 consecutive days. The rats were then sacrificed and samples of both steatosic liver and liver stimulated with infrared inductions were extracted for immediate processing via transmission electron microscopy.From both cell types transmission electron microphotographs were obtained at magnifications of 9500 X; these were subjected to morphometric studies to determine volumetric fractions of the following cell components: rough endoplasmic reticulum (RER), mitochondria, lipid and glycogen inclusions, euchromatin and heterochromatin. Likewise, cell and nuclear areas were quantified. Analysis of the results between steatosic and radiated hepatocytes revealed notable differences in all the cell components quantified. It is concluded that the effects of infrared stimulation with a dose of 6 J/cm2 brings about in the steatosic hepatocytes a microvesicular transformation in their ultrastructure and morphology, fundamentally in the considerable decrease in lipid infiltrations to 80%, which ultimately translates into a functional variation, thus representing an obvious impact produced by these infrared inductions.
Descritores: Hepatócitos/efeitos da radiação
Fígado Gorduroso/patologia
Raios Infravermelhos
Lasers
-Heterocromatina
Retículo Endoplasmático Rugoso
Microscopia Eletrônica de Transmissão
Modelos Animais de Doenças
Mitocôndrias
Limites: Animais
Feminino
Ratos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-961457
Autor: Bórquez, Juan Carlos; Montes, Nicolás; Díaz, Erik.
Título: Combatiendo el metabolismo de las células cancerosas mediante la activación de SIRT3 y el ejercicio físico / Combating tumor cells through SIRT3 activation and exercise
Fonte: Rev. méd. Chile;146(6):762-769, jun. 2018. graf.
Idioma: es.
Resumo: One of the main features of cancer is the high rate of cell proliferation and growth. To do this, cancer cells need to redirect their metabolism mainly towards anaerobic glycolysis and an increased mitochondrial glutamine energy metabolism. Sirtuins are cellular proteins with regulatory functions on metabolic pathways, genomic stability, apoptosis, longevity, inflammation, energy metabolism and oxidative stress. Sirtuins have emerged recently as a potential therapeutic option to treat several chronic diseases including cancer. This review summarizes the tumor suppressor function of Sirtuin 3 (SIRT3), highlighting its repressor effect on glycolytic metabolism, promoting mitochondrial metabolism and oxidative stress reduction. SIRT3 activation by exercise is particularly described since it may represent a potent tool for several types of cancer treatment.
Descritores: Exercício Físico/fisiologia
Sirtuína 3/fisiologia
Neoplasias/metabolismo
Neoplasias/terapia
-Espécies Reativas de Oxigênio/metabolismo
Estresse Oxidativo/fisiologia
Proteínas Supressoras de Tumor/fisiologia
Terapia por Exercício/métodos
Mitocôndrias/metabolismo
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1134436
Autor: Finol, Héctor J; García, Estefanie; González, Roschman; Sanchez, Elda E; Rodríguez-Acosta, Alexis.
Título: Qualitative and quantitative ultrastructural analysis of the mitochondria from adrenal gland cortex under the action of viperidae family snake venoms / Análisis ultrastructural cualitativo y cuantitativo de la mitocondria de la glándula adrenal bajo la acción de los venenos de serpientes de la familia viperidae
Fonte: Int. j. morphol;38(5):1271-1280, oct. 2020. tab, graf.
Idioma: en.
Resumo: SUMMARY: The Viperidae venoms are composed of a mixture of constituents with enzymatic and non-enzymatic actions, which act on ultrastructural components of cells and tissues. Here, the number of mitochondria, mitochondrial area and the number of mitochondrial cristae from adrenal glands cortex treated with snake venoms were tested after 3, 6 and 24 hours of venom injections. The mitochondria quantitative changes showed a statistically significant decrease, in the number of mitochondria past 3, 6 and 24 h. There was an increase in the mitochondrial area after 6 h, where Crotalus vegrandis venom did not present significant differences with Crotalus pifanorum or Bothrops venezuelensis venoms. After 24 h, there was an escalation of mitochondrial area in all tested venoms. The number of mitochondrial cristae after 3 h did not present important differences with the control treatment. After 6 h, the number of mitochondrial cristae initiated to decrease under the activities of the 3 venoms action, until 24 h of observation. In the qualitative observations it was possible to witness an intense damage of the mitochondria, with loss and swelling of membranes, disappearance of cristae and the appearance of myelin figures, which started at 3 h after the Crotalus and Bothrops venoms injections. These damages probably were due to cytotoxic effects of phospholipases, metalloproteases and/or other proteolytic activities present in Viperidae snake venoms, being more evident in Crotalus venoms. As far as we know, these results define a novel finding that suggest that Viperidae snake venoms are extremely toxic to mammalian mitochondria.

RESUMEN: Los venenos de Viperidae tienen acciones enzimáticas y no enzimáticas, que actúan sobre la estructura celular. Aquí se probaron, a las 3, 6 y 24 horas de la inyección del veneno, el número de mitocondrias, el área mitocondrial y el número de crestas mitocondriales de la corteza de las glándulas adrenales. Los cambios cuantitativos de las mitocondrias mostraron una disminución en el número de mitocondrias a las 3, 6 y 24 h. Hubo un aumento en el área mitocondrial a las 6 h, donde el veneno de la serpiente Crotalus vegrandis no presentó diferencias significativas con los venenos de Crotalus pifanorum o Bothrops venezuelensis. Después de 24 h, hubo un aumento del área mitocondrial en todos los venenos. El número de crestas mitocondriales a las 3 h no presentó alteraciones o diferencias importantes con el tratamiento de control. Después de 6 h, el número de crestas mitocondriales comenzó a disminuir bajo la acción de los 3 venenos, hasta las 24 h de observación. En las observaciones cualitativas se observó un daño intenso de las mitocondrias, con pérdida y edema de las membranas, desaparición de las cristae y aparición de figuras mielínicas, que comenzó a las 3 h después de las inyecciones de veneno de Crotalus y Bothrops. Estos daños se debieron factiblemente a los efectos citotóxicos de componentes proteolíticos de los venenos. Creemos que estos resultados definen un nuevo y original hallazgo, que sugiere que los venenos de serpiente Viperidae son extremadamente tóxicos para las mitocondrias de mamíferos.
Descritores: Venenos de Víboras/toxicidade
Viperidae/fisiologia
Glândulas Suprarrenais/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
-Glândulas Suprarrenais/ultraestrutura
Crotalus
Bothrops
Mitocôndrias/ultraestrutura
Limites: Animais
Camundongos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1153992
Autor: Chen, Danyan; Li, Li; Ren, Fang; Huang, Rongxi; Gan, Hua; Deng, Huacong; Wang, Hongman.
Título: Maternal hypothyroidism during pregnancy alters the function of the retinol-binding protein 4-mediated mitochondrial permeability conversion pore in the kidneys of offspring rats
Fonte: Clinics;76:e2096, 2021. tab, graf.
Idioma: en.
Projeto: Medical Science and Technology Innovation Project of Chongqing General Hospital.
Resumo: OBJECTIVES To determine the role of the RBP4/PiC/SIRT3 signaling pathway in the opening of the mitochondria permeability transition pore (mPTP) in offspring rats with hypothyroidism during pregnancy. METHODS Sixty Sprague-Dawley (SD) rats were employed in this study. Pregnancy was deemed successful when a sperm was found in the uterus. After one week of pregnancy, offspring rats were divided into the following groups: overall hypothyroidism group (OH group), subclinical hypothyroidism group (SCH group), and normal control group (CON group). The establishment of the hypothyroidism model was confirmed when the serum thyroid stimulating hormone (TSH) levels were higher than normal value and TT4 level was within the normal range. The renal mitochondria of offspring rats were extracted on the 14th postnatal day (P14) and 35th postnatal day (P35). RESULTS At P14, no significant differences in the degree of mPTP opening and expression of phosphoric acid carrier vector (PiC) were detected between the rats in the OH group and the SCH group. However, the expression level of silent mating-type information regulation 3 homolog (SIRT3) was markedly reduced. Retinol-binding protein 4 (RBP4) expression increased in the rats from the OH group, relative to that in those from the SCH group. At P35, the degree of mPTP opening and the expression levels of PiC and RBP4 in the OH group were higher than those in the SCH group. However, SIRT3 expression in the OH group was lower than that observed in the SCH group. CONCLUSION RBP4 plays an important role in early renal mitochondrial damage and renal impairment in rats suffering from hypothyroidism during pregnancy. The RBP4/PiC/SIRT3 pathway is thus involved in the opening of the renal mPTP in offspring rats with hyperthyroidism.
Descritores: Complicações na Gravidez
Hipotireoidismo/complicações
Hipotireoidismo/induzido quimicamente
Rim/metabolismo
Rim/patologia
Mitocôndrias
-Permeabilidade
Ratos Sprague-Dawley
Proteínas Plasmáticas de Ligação ao Retinol
Limites: Animais
Feminino
Gravidez
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: biblio-896986
Autor: Saibabu, Venkata; Singh, Shweta; Ansari, Moiz A; Fatima, Zeeshan; Hameed, Saif.
Título: Insights into the intracellular mechanisms of citronellal in Candida albicans: implications for reactive oxygen species-mediated necrosis, mitochondrial dysfunction, and DNA damage
Fonte: Rev. Soc. Bras. Med. Trop;50(4):524-529, July-Aug. 2017. graf.
Idioma: en.
Projeto: Science and Engineering Research Board.
Resumo: Abstract INTRODUCTION Citronellal (Cit) possesses antifungal activity and has possible implications for reactive oxygen species (ROS) generation in Candida albicans. In this study, the effects of Cit on ROS generation and the mechanisms by which Cit exerts anti-Candida effects were examined. METHODS A 2′,7′-dichlorodihydrofluorescein diacetate assay was used to assess oxidative damage. Cell necrosis was determined by flow cytometry after FITC-Annexin V staining. Mitochondrial function was studied based on mitochondrial potential, metabolic activity (MTT assay), and phenotypic susceptibility on a non-fermentable carbon source. Membrane intactness and DNA damage were estimated by a propidium iodide (PI) uptake assay and 4',6-diamidino-2-phenylindole (DAPI) staining. RESULTS ROS generation was enhanced in response to Cit, leading to necrosis (2%). Additional hallmarks of cell death in response to Cit, such as mitochondrial membrane depolarization and DNA damage, were also observed. Cit treatment resulted in dysfunctional mitochondria, as evidenced by poor labeling with the mitochondrial membrane potential-sensitive probe rhodamine B, reduced metabolic activity (61.5%), and inhibited growth on a non-fermentable carbon source. Furthermore, Cit induced DNA damage based on DAPI staining. These phenotypes were reinforced by RT-PCR showing differences in gene expression (30-60%) between control and Cit-treated cells. Finally, PI uptake in the presence of sodium azide confirmed non-intact membranes and suggested that Cit activity is independent of the energy status of the cell. CONCLUSIONS Cit possesses dual anticandidal mechanisms, including membrane-disruptive and oxidative damage. Taken together, our data demonstrated that cit could be used as a prominent antifungal drug.
Descritores: Candida albicans/efeitos dos fármacos
Espécies Reativas de Oxigênio
Monoterpenos/farmacologia
Aldeídos/farmacologia
Antifúngicos/farmacologia
-Dano ao DNA
Monoterpenos Acíclicos
Mitocôndrias/efeitos dos fármacos
Necrose
Limites: Humanos
Responsável: BR1.1 - BIREME


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Id: biblio-950750
Autor: Pieme, Constant Anatole; Santosh, Guru Kumar; Tekwu, Emmanuel Mouafo; Askun, Tülin; Aydeniz, Hatice; Ngogang, Jeanne Yonkeu; Bhushan, Shashi; Saxena, Ajit Kumar.
Título: Fruits and barks extracts of Zanthozyllum heitzii a spice from Cameroon induce mitochondrial dependent apoptosis and Go/G1 phase arrest in human leukemia HL-60 cells
Fonte: Biol. Res;47:1-13, 2014. ilus, graf, tab.
Idioma: en.
Resumo: BACKGROUND: Zanthoxylum heitzii is a spice used to prepare several dishes and to treat tumors, syphilis, malaria, cardiac palpitations, urogenital infections in the west region of Cameroon, but the antitumor mechanisms and chemical composition are not yet investigated. This study was aimed to determine the antiproliferative effects of four extracts from the fruits and barks of Zanthoxyllum heitzii (Rutaceae) on apoptosis in human promyelocytic cells, their mechanisms and the chemical composition. The 3-(4, 5-dimethylthiazole-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to determine the fifty percent inhibition (IC50) concentration of the cell lines after treatment. The effect on morphology was observed using a light or fluorescence microscopy. The rate of apoptosis and the cell cycle were measured using flow cytometry (FCM). The phytochemical analysis of the extract was carried with HPLC/MS methods. RESULTS: The phytochemical analysis of the extracts indicated the presence of four known polyphenols (Syringic acid, Juglon, Luteolin and Myricetin) in both fruits and barks of Z. heitzii but in different quantities. Syringic acid and Myricetin concentrations were between 17-21 fold higher in the fruits than the stem bark. Rhamnetin (393.35 µg/mL) and Oleuropein (63.10 µg/mL) were identified only in the stem barks of Z. heitzii. Among the four extracts tested for cytotoxicity properties, only the methanol extract of fruits and barks significantly inhibited cell proliferation of HL-60 cells with IC50 value of 20 µg/mL and 12 µg/mL respectively. HL-60 cells treated with Z. heitzii extracts significantly produced reactive oxygen species (ROS) with concurrent loss of mitochondrial membrane potential (MMP). Modifications in the DNA distribution and enhanced of G1/G0 phase cell cycle arrest were observed in a concentration dependent manner. CONCLUSIONS: Polyphenols from Z. heitzii plant exert inhibitory effect on HL-60 cells through the reactive oxygen species (ROS) generation, loss of mitochondrial membrane potential and cell cycle destabilization.
Descritores: Apoptose/efeitos dos fármacos
Casca de Planta/química
Zanthoxylum/química
Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos
Frutas/química
Mitocôndrias/fisiologia
-Espectrometria de Massas
Sais de Tetrazólio
Tiazóis
Camarões
Extratos Vegetais/isolamento & purificação
Extratos Vegetais/química
Cromatografia Líquida de Alta Pressão
Especiarias/análise
Espécies Reativas de Oxigênio/análise
Células HL-60
Concentração Inibidora 50
Proliferação de Células/efeitos dos fármacos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Polifenóis/análise
Citometria de Fluxo
Microscopia de Fluorescência
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950770
Autor: Soto-Urquieta, María G; López-Briones, Sergio; Pérez-Vázquez, Victoriano; Saavedra-Molina, Alfredo; González-Hernández, Gloria A; Ramírez-Emiliano, Joel.
Título: Curcumin restores mitochondrial functions and decreases lipid peroxidation in liver and kidneys of diabetic db/db mice
Fonte: Biol. Res;47:1-8, 2014. graf.
Idioma: en.
Resumo: BACKGROUND: Nitrosative and oxidative stress play a key role in obesity and diabetes-related mitochondrial dysfunction. The objective was to investigate the effect of curcumin treatment on state 3 and 4 oxygen consumption, nitric oxide (NO) synthesis, ATPase activity and lipid oxidation in mitochondria isolated from liver and kidneys of diabetic db/db mice. RESULTS: Hyperglycaemia increased oxygen consumption and decreased NO synthesis in liver mitochondria isolated from diabetic mice relative to the control mice. In kidney mitochondria, hyperglycaemia increased state 3 oxygen consumption and thiobarbituric acid-reactive substances (TBARS) levels in diabetic mice relative to control mice. Interestingly, treating db/db mice with curcumin improved or restored these parameters to normal levels; also curcumin increased liver mitochondrial ATPase activity in db/db mice relative to untreated db/db mice. CONCLUSIONS: These findings suggest that hyperglycaemia modifies oxygen consumption rate, NO synthesis and increases TBARS levels in mitochondria from the liver and kidneys of diabetic mice, whereas curcumin may have a protective role against these alterations.
Descritores: Peroxidação de Lipídeos/efeitos dos fármacos
Curcumina/farmacologia
Diabetes Mellitus Tipo 2/dietoterapia
Rim/efeitos dos fármacos
Fígado/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
-Consumo de Oxigênio/efeitos dos fármacos
Peso Corporal/efeitos dos fármacos
Mitocôndrias Hepáticas/efeitos dos fármacos
Mitocôndrias Hepáticas/enzimologia
Adenosina Trifosfatases/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Respiração Celular/efeitos dos fármacos
Suplementos Nutricionais
Diabetes Mellitus Tipo 2/complicações
Diabetes Mellitus Tipo 2/fisiopatologia
Modelos Animais de Doenças
Seleção Artificial
Genótipo
Hiperglicemia/dietoterapia
Hiperglicemia/etiologia
Mitocôndrias/enzimologia
Óxido Nítrico/análise
Óxido Nítrico/metabolismo
Limites: Animais
Masculino
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-985704
Autor: Sepúlveda, Rodrigo A; Ortega, Marcos; Donoso, Natalia; Jara, Aquiles.
Título: Intoxicación por ácido acetilsalicílico, fisiopatología y manejo / Physiopathology and management of acetylsalicylic acid intoxication
Fonte: Rev. méd. Chile;146(11):1309-1316, nov. 2018. tab, graf.
Idioma: es.
Resumo: Acetylsalicylic acid (ASA) intoxication is potentially lethal. After ingestion, AAS is rapidly transformed into salicylic acid that dissociates into an hydrogen ion plus salicylate. Salicylate is the main form of AAS in the body and produces multiple alterations. Initially, the stimulation of the ventilatory center promotes a respiratory alkalosis. Then, the mitochondrial dysfunction induced by salicylate, will generate a progressive metabolic acidosis due to the accumulation of ketoacids, lactic acid and dicarboxylic acids among others. Another alterations include hydro electrolytic disorders, gastrointestinal lesions, neurological involvement, ototoxicity and coagulopathy. The correct handling of acetylsalicylic acid intoxication requires an thorough knowledge of its pharmacokinetics and pharmacodynamics. Treatment consists in life support measures, gastric lavage, activated charcoal and urinary alkalization to promote the excretion of salicylates. In some occasions, it will be necessary to start renal replacement therapy as soon as possible.
Descritores: Aspirina/envenenamento
Aspirina/metabolismo
Fibrinolíticos/envenenamento
Fibrinolíticos/metabolismo
Overdose de Drogas/fisiopatologia
Overdose de Drogas/terapia
-Acidose/induzido quimicamente
Equilíbrio Hidroeletrolítico/efeitos dos fármacos
Aspirina/administração & dosagem
Overdose de Drogas/metabolismo
Hipoglicemia/induzido quimicamente
Hipotensão/induzido quimicamente
Mitocôndrias/efeitos dos fármacos
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950809
Autor: Lee, Seahyoung; Yun, Ina; Ham, Onju; Lee, Se-Yeon; Lee, Chang Yeon; Park, Jun-Hee; Lee, Jiyun; Seo, Hyang-Hee; Choi, Eunhyun; Hwang, Ki-Chul.
Título: Suppression of miR-181 a attenuates H2O2-induced death of mesenchymal stem cells by maintaining hexokinase II expression
Fonte: Biol. Res;48:1-7, 2015. graf.
Idioma: en.
Projeto: Korea Science and Engineering Foundation; . Ministry of Health and Welfare. Grant from the Korea Health 21 R&´D Project.
Resumo: BACKGROUND: Low survival rate of transplanted cells compromises the efficacy of cell therapy. Hexokinase II (HKII) is known to have anti-apoptotic activity through its interaction with mitochondria. The objective was to identify miRNAs targeting HKII and investigate whether miRNA-mediated modulation of HKII could improve the survival of mesenchymal stem cells (MSCs) exposed to H2O2. The expression of HKII in MSCs exposed to H2O2 was evaluated, and HKII-targeting miRNA was screened based on miRNA-target prediction databases. The effect of H2O2 on the expression of the selected HKII-targeting miRNA was examined and the effect of modulation of the selected HKII-targeting miRNA using anti-miRNA on H2O2-induced apoptosis of MSC was evaluated. RESULTS: H2O2 (600 µM) induced cell death of MSCs and decreased mitochondrial HKII expression. We have identified miR-181a as a HKII-targeting miRNA and H2O2 increased the expression of miR-181a in MSCs. Delivery of anti-miR-181a, which neutralizes endogenous miR-181a, significantly attenuated H2O2-induced decrease of HKII expression and disruption of mitochondrial membrane potential, improving the survival of MSCs exposed to H2O2. CONCLUSIONS: These findings suggest that H2O2-induced up-regulation of miR-181a contributes to the cell death of MSCs by down-regulating HKII. Neutralizing miR-181a can be an effective way to prime MSCs for transplantation into ischemic tissues.
Descritores: Apoptose
MicroRNAs/metabolismo
Células-Tronco Mesenquimais/patologia
Glioma/patologia
Hexoquinase/metabolismo
Peróxido de Hidrogênio/toxicidade
-Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/metabolismo
Diferenciação Celular
Movimento Celular
Sobrevivência Celular
Espécies Reativas de Oxigênio
Semaforinas/genética
Semaforinas/metabolismo
MicroRNAs/antagonistas & inibidores
Células-Tronco Mesenquimais/efeitos dos fármacos
Células-Tronco Mesenquimais/enzimologia
Reação em Cadeia da Polimerase em Tempo Real
Glioma/metabolismo
Peróxido de Hidrogênio/administração & dosagem
Mitocôndrias/enzimologia
Invasividade Neoplásica
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: CL1.1 - Biblioteca Central


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Id: lil-666936
Autor: Cavalcanti, José Luiz de Sá; Engelhardt, Eliasz.
Título: Aspectos da fisiopatologia da doença de Alzheimer esporádica / Pathophysiological features of sporadic Alzheimer's disease
Fonte: Rev. bras. neurol;48(4):21-29, out.-dez. 2012. ilus.
Idioma: pt.
Resumo: A doença de Alzheimer (DA) é a forma de demência degenerativa esporádica mais comum. Caracteristicamente ocorre expressiva perda neuronal progressiva em locais específicos nas pessoas atingidas. O distúrbio degenerativo progressivo se caracteriza pela perda de sinapses, de neurônios cerebrais e por depósitos de fibrilas de peptídeos de beta-amilóide extraneuronais, constituindo as placas senis e a presença de agregados intraneuronais da proteína tau, formando os emaranhados neurofibrilares. Fatores genéticos, metabólicos, neuroinflamação, alterações mitocondriais, distúrbios vasculares e processos oxidativos estão envolvidos no desencadear e manutenção de várias doenças neurodegenerativas, incluindo a DA. Todas essas alterações participam no processo fisiopatológico da doença. O objetivo desta revisão é mostrar a associação das várias causas subjacentes ao processo fisiopatológico da DA, com vistas ao desenvolvimento de marcadores biológicos e estratégias terapêuticas.

Alzheimer's disease (AD) is the most common form of sporadic degenerative dementia. Characteristically there is an expressive neuronal loss in specific sites in the affected persons. The progressive degenerative disorder is characterized by synaptic loss, of brain neurons, and by extraneuronal deposition of beta-amyloid fibrils, constituting the senile plaques, and the presence of intraneuronal aggregates of tau protein, forming the neurofibrillary tangles. Genetic factors, metabolic, neuroinflammation, mitochondrial disturbances, vascular disorders and oxidative processes are involved in the onset and maintenance of several neurodegenerative disorders, including AD. All these disturbances participate in the pathophysiological process of the disease. The aim of this review is to show the association of the varied causes underlying the pathophysiological process of AD, having in view the development of biological markers and therapeutic strategies.
Descritores: Transtornos Cognitivos
Doença de Alzheimer/etiologia
Doença de Alzheimer/fisiopatologia
-Sinapses
Peptídeos beta-Amiloides
Estresse Oxidativo
Doença de Alzheimer/genética
Mitocôndrias
Degeneração Neural
Limites: Humanos
Idoso
Responsável: BR14.1 - Biblioteca Central



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