Browsing by Author "Velarde Aliaga, María Victoria"

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    Antioxidant and anti hyperglycemic role of wine grape powder in rats fed with a high fructose diet
    (2015) Hernández-Salinas, Romina.; Decap, Valerie.; Leguina-Ruzzi, Alberto; Cáceres, Patricio.; Pérez, Druso.; Urquiaga Reus, Inés; Iturriaga Agüera, Rodrigo; Velarde Aliaga, María Victoria
    Abstract Background Metabolic syndrome is a growing worldwide health problem. We evaluated the effects of wine grape powder (WGP), rich in antioxidants and fiber, in a rat model of metabolic syndrome induced by a high fructose diet. We tested whether WGP supplementation may prevent glucose intolerance and decrease oxidative stress in rats fed with a high fructose diet. Methods Male Sprague–Dawley rats weighing 180 g were divided into four groups according to their feeding protocols. Rats were fed with control diet (C), control plus 20 % WGP (C + WGP), 50 % high fructose (HF) or 50 % fructose plus 20 % WGP (HF + WGP) for 16 weeks. Blood glucose, insulin and triglycerides, weight, and arterial blood pressure were measured. Homeostasis model assessment (HOMA) index was calculated using insulin and glucose values. A glucose tolerance test was performed 2 days before the end of the experiment. As an index of oxidative stress, thiobarbituric acid reactive substances (TBARS) level was measured in plasma and kidney, and superoxide dismutase was measured in the kidney. Results Thiobarbituric acid reactive substances in plasma and renal tissue were significantly higher when compared to the control group. In addition, the area under the curve of the glucose tolerance test was higher in HF fed animals. Furthermore, fasting blood glucose, plasma insulin levels, and the HOMA index, were also increased. WGP supplementation prevented these alterations in rats fed with the HF diet. We did not find any significant difference in body weight or systolic blood pressure in any of the groups. Conclusions Our results show that WGP supplementation prevented hyperglycemia, insulin resistance and reduced oxidative stress in rats fed with HF diet. We propose that WGP may be used as a supplement in human food as well.Abstract Background Metabolic syndrome is a growing worldwide health problem. We evaluated the effects of wine grape powder (WGP), rich in antioxidants and fiber, in a rat model of metabolic syndrome induced by a high fructose diet. We tested whether WGP supplementation may prevent glucose intolerance and decrease oxidative stress in rats fed with a high fructose diet. Methods Male Sprague–Dawley rats weighing 180 g were divided into four groups according to their feeding protocols. Rats were fed with control diet (C), control plus 20 % WGP (C + WGP), 50 % high fructose (HF) or 50 % fructose plus 20 % WGP (HF + WGP) for 16 weeks. Blood glucose, insulin and triglycerides, weight, and arterial blood pressure were measured. Homeostasis model assessment (HOMA) index was calculated using insulin and glucose values. A glucose tolerance test was performed 2 days before the end of the experiment. As an index of oxidative stress, thiobarbituric acid reactive substances (TBARS) level was measured in plasma and kidney, and superoxide dismutase was measured in the kidney. Results Thiobarbituric acid reactive substances in plasma and renal tissue were significantly higher when compared to the control group. In addition, the area under the curve of the glucose tolerance test was higher in HF fed animals. Furthermore, fasting blood glucose, plasma insulin levels, and the HOMA index, were also increased. WGP supplementation prevented these alterations in rats fed with the HF diet. We did not find any significant difference in body weight or systolic blood pressure in any of the groups. Conclusions Our results show that WGP supplementation prevented hyperglycemia, insulin resistance and reduced oxidative stress in rats fed with HF diet. We propose that WGP may be used as a supplement in human food as well.Abstract Background Metabolic syndrome is a growing worldwide health problem. We evaluated the effects of wine grape powder (WGP), rich in antioxidants and fiber, in a rat model of metabolic syndrome induced by a high fructose diet. We tested whether WGP supplementation may prevent glucose intolerance and decrease oxidative stress in rats fed with a high fructose diet. Methods Male Sprague–Dawley rats weighing 180 g were divided into four groups according to their feeding protocols. Rats were fed with control diet (C), control plus 20 % WGP (C + WGP), 50 % high fructose (HF) or 50 % fructose plus 20 % WGP (HF + WGP) for 16 weeks. Blood glucose, insulin and triglycerides, weight, and arterial blood pressure were measured. Homeostasis model assessment (HOMA) index was calculated using insulin and glucose values. A glucose tolerance test was performed 2 days before the end of the experiment. As an index of oxidative stress, thiobarbituric acid reactive substances (TBARS) level was measured in plasma and kidney, and superoxide dismutase was measured in the kidney. Results Thiobarbituric acid reactive substances in plasma and renal tissue were significantly higher when compared to the control group. In addition, the area under the curve of the glucose tolerance test was higher in HF fed animals. Furthermore, fasting blood glucose, plasma insulin levels, and the HOMA index, were also increased. WGP supplementation prevented these alterations in rats fed with the HF diet. We did not find any significant difference in body weight or systolic blood pressure in any of the groups. Conclusions Our results show that WGP supplementation prevented hyperglycemia, insulin resistance and reduced oxidative stress in rats fed with HF diet. We propose that WGP may be used as a supplement in human food as well.
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    Basic fibroblast growth factor reduces functional and structural damage in chronic kidney disease
    (2014) Velarde Aliaga, María Victoria; Vio Lagos, Carlos P.
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    Boldine Improves Kidney Damage in the Goldblatt 2K1C Model Avoiding the Increase in TGF-β
    (2018) Gómez Órdenes, Gonzalo Ignacio; Velarde Aliaga, María Victoria
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    Cyclooxygenase-2 Induction by Bradykinin in Aortic Vascular Smooth Muscle Cells
    (2006) Rodríguez, Javier; Vio Lagos, Carlos P.; Velarde Aliaga, María Victoria
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    Dehydroepiandrosterone Prevents the Aggregation of Platelets Obtained from Postmenopausal Women with Type 2 Diabetes Mellitus through the Activation of the PKC/eNOS/NO Pathway
    (2012) Muñoz Sola, Yanira Elizabeth del Carmen.; Gómez Órdenes, Gonzalo Ignacio; Velarde Aliaga, María Victoria
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    Diabetes alters the involvement of myofibroblasts during periodontal wound healing
    (2020) Retamal, I.; Hernández Salinas, Romina; Velarde Aliaga, María Victoria; Oyarzun, A.; Martínez, Constanza; Gonzalez, M. J.; Martínez Castillo, Jorge; Smith Ferrer, Patricio
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    Effect of ischemic acute renal damage on the expression of COX-2 and oxidative stress-related elements in rat kidney
    (2007) Villanueva Morales, Irma Sandra.; Céspedes Fierro, Carlos Mauricio.; Vio Lagos, Carlos P.; Velarde Aliaga, María Victoria
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    Effect of Tamoxifen and Retinoic Acid on Bradykinin Induced Proliferation in MCF-7 Cells
    (2009) Paola Searovic; Alonso, Marcelo; Oses, Carolina; Pereira Flores, K.; Velarde Aliaga, María Victoria; Sáez Steeger, Claudia
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    Effects of ascorbic acid on spermatogenesis and sperm parameters in diabetic rats
    (2017) Aguirre, M.; Velarde Aliaga, María Victoria; Moreno Mauro, Ricardo D.
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    EPAC expression and function in cardiac fibroblasts and myofibroblasts.
    (2013) Olmedo, I.; Velarde Aliaga, María Victoria
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    Estudio de marcadores de disfunción endotelial en el síndrome metabólico : evaluación de la vía RhoA/ROCK como posible eje de señalización
    (2015) Leguina Ruzzi, Alberto Andrés; Sáez S., Claudia; Velarde Aliaga, María Victoria; Pontificia Universidad Católica de Chile. Facultad de Medicina
    El Síndrome Metabólico (SM) es un agregado de condiciones cardio-metabólicas que en cronicidad involucra patologías tales como la obesidad, diabetes e hipertensión arterial (HTA), aumentando considerablemente el riesgo de desarrollar enfermedades cardiovasculares (ECV). La aterosclerosis es el denominador común de las patologías que desencadenan los eventos cardiovasculares y la disfunción endotelial (DE) es la alteración base del proceso aterosclerótico. La prevalencia mundial del SM ha aumentado progresivamente, alcanzando alrededor del 25% de la población adulta. Existen datos clínicos de una población mas joven que califica para SM por mostrar un aumento de la circunferencia de la cintura y sobrepeso junto con niveles elevados de triglicéridos plasmáticos. En este grupo de sujetos jóvenes con SM se desconoce la presencia de marcadores de daño endotelial e inflamatorios similares a los que presentan pacientes adultos sobre 50 años con diabetes tipo 2 e hipertensión. En este último grupo de adultos, se han reportado niveles elevados de citoquinas inflamatorias tales como IL-6, de ácidos grasos, específicamente el ácido palmítico (AP), hiper-insulinemia y alteraciones relacionadas con DE y, solo en un reporte, se ha mencionado la sobre-activación de la vía RhoA/ROCK.En base a lo expuesto planteamos como hipótesis que: IL-6, insulina y AP son moléculas que se encuentran elevadas en sujetos con SM sin diabetes tipo 2 o hipertensión arterial, y pueden inducir DE mediada por la activación de RhoA/ROCK. Para poner a prueba nuestro postulado propusimos tres estrategias que involucran estudios ex–vivo, in–vitro e in–vivo. Los estudios ex–vivo se realizaron en sujetos adultos jóvenes que consultaron por sobrepeso pero calificaron para SM por presentar aumento del contorno de cintura y dislipidemia. Nuestros resultados mostraron que el grupo de sujetos evaluado tiene, además de niveles de LDL-c elevados y HDL-c bajos, altos niveles de IL-6, insulina y AP, aumento de marcadores de DE tales como MCP-1, sICAM-1, aumento de marcadores de estrés oxidativo (AOPP y TBARS), menor biodisponibilidad de óxido nítrico (ON) y una sobre activación de RhoA/ROCK en leucocitos en comparación a sujetos sanos. Aunque dentro de rango normales, se encontró además, mayores niveles plasmáticos de ácido úrico, menores niveles creatinina y un moderado estado de hiper-coagulabilidad en comparación con individuos controles.El estudio in-vitro se llevó a cabo en células endoteliales de cordón umbilical estimuladas con concentración similares a las encontradas en sujetos con SM de IL-6, insulina y AP, con el objetivo de evaluar la participación de RhoA/ROCK en el daño endotelial inducido por estas moléculas. Los resultados mostraron que la combinación de IL-6, insulina y AP activa la vía RhoA/ROCK y altera la señalización de Akt y ERK. Adicionalmente, se reducen los niveles de ON y la actividad de eNOS, junto a un aumento de los niveles de marcadores de estrés oxidativo. Se observaron cambios en la estructura de actina y de VEcaderina y alteraciones en la citoarquitectura de la monocapa celular, acompañado de un aumento de la actividad de MMP9 intracelular. La triple estimulación aumentó la adhesión plaquetaria, la actividad pro-coagulante, la liberación de Factor de Von Willenbrand (FVW), MCP-1, siCAM-1, E-selectina y la acumulación intracelular de lípidos. Todas estas alteraciones a excepción de los niveles de FVW y la actividad pro-coagulante parecen ser mediadas por la sobre-activación de RhoA/ROCK ya que se evitaron al adicionar el inhibidor Y-27632.La participación de RhoA/ROCK en relación a características de SM se evaluó en un modelo de ratas alimentadas con una dieta rica en AP por 14 semanas con y sin la administración de Fasudil, un inhibidor de RhoA/ROCK, por las dos últimas semanas. Los resultados muestran que la dieta alta en grasa indujo características SM tales como: sobrepeso, mayor circunferencia abdominal y dislipidemia. A las 14 semanas de dieta los animales tuvieron presión sistólica elevada, altos niveles de triglicéridos, colesterol y glicemia, en comparación a los animales controles pero dentro de los rangos de normalidad. La dieta alta en grasa indujo además altos niveles de insulina, IL-6, aumento de tejido adiposo extra-peritoneal, marcadores de estrés oxidativo (TBARS y AOPP), siCAM-1, sCD40L, ácido úrico y niveles reducidos de ON. La administración de Fasudil por dos semanas, revirtió las alteraciones observadas. El análisis de las aortas de los animales alimentados con dieta rica en AP muestra una mayor infiltración grasa y un aumento de la actividad de RhoA/ROCK, de E-selectina, una disminución de la actividad de Akt, eNOS y de los niveles de Nrf2 comparados con las aortas de los animales alimentados con dieta control. Los animales tratados con Fasudil mostraron una reducción de las alteraciones mencionadas. A pesar de la presencia de alteraciones metabólicas, la dieta alta en grasa no indujo diabetes ni HTA en los animales durante el periodo estudiado.Consideramos que los resultados de esta tesis entregan evidencias sobre la participación de RhoA/ROCK en las alteraciones relacionadas a la DE asociadas a SM y demuestra el rol del AP, IL-6 e insulina como componentes que, al estar elevados en pacientes con SM, promueven DE. Adicionalmente, creemos que los resultados obtenidos entregan información relevante para sujetos jóvenes con SM que, por no mostrar síntomas relacionadas con patologías tales como diabetes tipo 2 o hipertensión, desconocen que ya presentan signos relacionados con mayor riesgo cardiovascular.
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    Evaluación del efecto renoprotector de angiotensina (1-7) en insuficiencia renal crónica
    (2014) Rivera Camaño, Juan Carlos F.; Vio Lagos, Carlos P.; Velarde Aliaga, María Victoria; Pontificia Universidad Católica de Chile. Facultad de Ciencias Biológicas
    La insuficiencia renal crónica (CKD) es un problema de salud pública a nivel mundial, que conduce a enfermedades cardiovasculares en estados avanzados y a la muerte de los pacientes. Angiotensina(1-7) (Ang(1-7)) un péptido del sistema renina angiotensina que actúa a través del receptor Mas, tiene efectos opuestos a angiotensina II, tales como disminución de la presión arterial, efectos anti-inflamatorios y anti-proliferativos. Debido a que angiotensina II está incrementada en la CKD, nosotros proponemos que la activación del receptor Mas por Ang(1-7) reduce la progresión de la CKD. La CKD fue inducida en ratas macho Sprague Dawley. Tres semanas después, los animales recibieron los siguientes tratamientos: CKD+Ang(1-7) (6 μg/kg/h), CKD+A779 (antagonista del receptor Mas) (2 μg/kg/h), CKD+Ang(1-7)+A779, más un grupo CKD y otro sham; las drogas se administraron a través de bombas osmóticas. Se analizó la presión arterial sistólica (PAS), en tanto, la función renal fue evaluada a través de la creatinina plasmática, clearance de creatinina (CCr), proteinuria y la razón proteinuria/creatininuria (RPC). El daño morfológico se analizó por el Score túbulo-intersticial con tinción hematoxilina-eosina para la dilatación tubular, depósito de proteína tubular e infiltrado túbulo-intersticial. Colágeno III, miofibroblastos, macrófagos ED-1 (+) y osteopontina por inmunohistoquímica. La expresión de la proteína de fibronectina, el receptor AT1 y Mas se midió mediante western blot.La PAS, FE de K+ y Na+ mostraron una tendencia a reducirse con Ang(1-7) en relación a las ratas con CKD, otros parámetros como CCr, proteinuria y la RPC se normalizaron en CKD+Ang(1-7) comparado con CKD. El daño morfológico fué menor en CKD+Ang(1-7), en contraste con CKD donde se observó el mayor daño. La expresión de fibronectina aumentó en CKD+A779, y se mantuvo en niveles bajos en CKD+Ang(1-7) comparado con el sham. La expresión de los receptores AT1 y Mas no se modificó en ninguno de los grupos. Estos resultados sugieren que Ang(1-7) posee un efecto protector en el riñón, siendo gran parte de estos efectos no mediados por el receptor Mas.
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    Glucose increases intracellular free Ca2+ in tanycytes via ATP released through connexin 43 hemichannels
    (Wiley Periodicals, Inc., 2012) Orellana Roca, Juan Andrés; Sáez Pedraza, Pablo José; Cortés-Campos, Christian; Elizondo, Roberto J.; Shoji Sánchez, Kenji Fabricio; Contreras Duarte, Susana de las Mercedes; Figueroa, Vania; Velarde Aliaga, María Victoria; Jiang, Jean X.; Nualart, Francisco; Sáez, Juan Carlos; García, María A.
    The ventromedial hypothalamus is involved in regulating feeding and satiety behavior, and its neurons interact with specialized ependymal-glial cells, termed tanycytes. The latter express glucose-sensing proteins, including glucose transporter 2, glucokinase, and ATP-sensitive K+ (KATP) channels, suggesting their involvement in hypothalamic glucosensing. Here, the transduction mechanism involved in the glucose-induced rise of intracellular free Ca2+ concentration ([Ca2+]i) in cultured beta-tanycytes was examined. Fura-2AM time-lapse fluorescence images revealed that glucose increases the intracellular Ca2+ signal in a concentration-dependent manner. Glucose transportation, primarily via glucose transporters, and metabolism via anaerobic glycolysis increased connexin 43 (Cx43) hemichannel activity, evaluated by ethidium uptake and whole cell patch clamp recordings, through a KATP channel-dependent pathway. Consequently, ATP export to the extracellular milieu was enhanced, resulting in activation of purinergic P2Y1 receptors followed by inositol trisphosphate receptor activation and Ca2+ release from intracellular stores. The present study identifies the mechanism by which glucose increases [Ca2+]i in tanycytes. It also establishes that Cx43 hemichannels can be rapidly activated under physiological conditions by the sequential activation of glucosensing proteins in normal tanycytes
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    Hemichannels in the Neurovascular Unit and White Matter Under Normal and Inflamed Conditions
    (2011) Orellana Roca, Juan Andrés; Figueroa, Xavier; Sánchez Riquelme, Helmuth Alberto; Contreras Duarte, Susana de las Mercedes; Velarde Aliaga, María Victoria; Sáez, Juan Carlos
    In the normal brain, cellular types that compose the neurovascular unit, including neurons, astrocytes and endothelial cells express pannexins and connexins, which are protein subunits of two families that form plasma membrane channels. Most available evidence in mammals indicated that endogenously expressed pannexins only form hemichannels, and connexins form both gap junction channels and hemichannels. While gap junction channels connect the cytoplasm of contacting cells and coordinate electrical and metabolic activities, hemichannels communicate intra- and extracellular compartments and serve as diffusional pathways for ions and small molecules. Here, evidence supporting the functional role of hemichannels in the neurovascular unit and white matter under physiological and pathological conditions are reviewed. A sub-threshold acute pathological threatening condition ( e. g., stroke and brain infection) leads to glial cell activation, which maintains an active defense and restores the normal function of the neurovascular unit. However, if the stimulus is deleterious, microglia and the endothelium become overactivated, both releasing bioactive molecules ( e. g., glutamate, cytokines, prostaglandins and ATP) that increase the activity of astroglial hemichannels, reducing the astrocyte neuroprotective functions, and further reducing neuronal cell viability. Moreover, ATP is known to contribute to myelin degeneration of axons. Consequently, hemichannels might play a relevant role in the excitotoxic response of oligodendrocytes observed in ischemia and encephalomyelitis. Regulated changes in hemichannel permeability in healthy brain cells can have positive consequences in terms of paracrine/autocrine signaling, whereas persistent changes in cells affected by neurological disorders can be detrimental. Therefore, blocking hemichannels expressed by glial cells and/or neurons of the inflamed central nervous system might prevent neurovascular unit dysfunction and neurodegeneration.
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    High Glucose Increases B1-Kinin Receptor Expression and Signaling in Endothelial Cells
    (2006) Rodríguez, A.; Boric P., Mauricio; Velarde Aliaga, María Victoria
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    Hipertrofia Vascular: Un Mismo Mensaje, Una Diferente Interpretacion
    (2001) Velarde Aliaga, María Victoria
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    Hypoxia in High Glucose Followed by Reoxygenation in Normal Glucose Reduces the Viability of Cortical Astrocytes Through Increased Permeability of Connexin 43 Hemichannels
    (2010) Orellana Roca, Juan Andrés; Hernández Trejo, Diego Eduardo.; Velarde Aliaga, María Victoria; Sáez, Juan Carlos
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    Increased Kinin Levels and Decreased Responsiveness to Kinins During Aging
    (2005) Pérez V; Velarde Aliaga, María Victoria
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    Increased RhoA/Rho-Kinase Activity and Markers of Endothelial Dysfunction in Young Adult Subjects with Metabolic Syndrome
    (2015) Leguina-Ruzzi, Alberto; Pereira Garcés, Jaime Ignacio; Pereira-Flores, Karla; Valderas Igor, Juan Patricio; Mezzano, Diego; Velarde Aliaga, María Victoria; Sáez S., Claudia