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Id: biblio-1160748
Título: Molecular mechanisms in cell signaling and gene expression. Abstracts. November 6-7, 2013. Buenos Aires, Argentina / Molecular mechanisms in cell signaling and gene expression. Abstracts. November 6-7, 2013. Buenos Aires, Argentina.
Fonte: Biocell;37 Suppl:13-53, 2013 Nov.
Idioma: es.
Descritores: Expressão Gênica
Transdução de Sinais
-Animais
Humanos
Tipo de Publ: Congresso
Overall
Overall
Overall
Responsável: AR5.1 - Centro de Gestión del Conocimiento y las Comunicaciónes


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Id: biblio-838658
Autor: Chodari, Leila; Mohammadi, Mustafa; Mohaddes, Gisou; Alipour, Mohammad Reza; Ghorbanzade, Vajiheh; Dariushnejad, Hassan; Mohammadi, Shima.
Título: Testosterone and Voluntary Exercise, Alone or Together Increase Cardiac Activation of AKT and ERK1/2 in Diabetic Rats / Testosterona e Exercício Voluntário, Individualmente ou em Conjunto, Aumentam a Ativação Cardíaca de AKT e ERK1/2 em Ratos Diabéticos
Fonte: Arq. bras. cardiol;107(6):532-541, Dec. 2016. tab, graf.
Idioma: en.
Resumo: Abstract Background: Impaired angiogenesis in cardiac tissue is a major complication of diabetes. Protein kinase B (AKT) and extracellular signal regulated kinase (ERK) signaling pathways play important role during capillary-like network formation in angiogenesis process. Objectives: To determine the effects of testosterone and voluntary exercise on levels of vascularity, phosphorylated Akt (P- AKT) and phosphorylated ERK (P-ERK) in heart tissue of diabetic and castrated diabetic rats. Methods: Type I diabetes was induced by i.p injection of 50 mg/kg of streptozotocin in animals. After 42 days of treatment with testosterone (2mg/kg/day) or voluntary exercise alone or in combination, heart tissue samples were collected and used for histological evaluation and determination of P-AKT and P-ERK levels by ELISA method. Results: Our results showed that either testosterone or exercise increased capillarity, P-AKT, and P-ERK levels in the heart of diabetic rats. Treatment of diabetic rats with testosterone and exercise had a synergistic effect on capillarity, P-AKT, and P-ERK levels in heart. Furthermore, in the castrated diabetes group, capillarity, P-AKT, and P-ERK levels significantly decreased in the heart, whereas either testosterone treatment or exercise training reversed these effects. Also, simultaneous treatment of castrated diabetic rats with testosterone and exercise had an additive effect on P-AKT and P-ERK levels. Conclusion: Our findings suggest that testosterone and exercise alone or together can increase angiogenesis in the heart of diabetic and castrated diabetic rats. The proangiogenesis effects of testosterone and exercise are associated with the enhanced activation of AKT and ERK1/2 in heart tissue.

Resumo Fundamento: Angiogênese prejudicada em tecido cardíaco é uma das principais complicações das diabetes. As vias de sinalização da proteína-quinase B (AKT) e a quinase regulada por sinal extracelular (ERK) exercem um importante papel durante a formação de uma rede similar à capilar no processo de angiogênese. Objetivos: Determinar os efeitos da testosterona e exercícios voluntários sobre os níveis de vascularidade, AKT fosforilada (P- AKT) e ERK fosforilada (P-ERK) sobre o tecido cardíaco de ratos diabéticos e castrados diabéticos. Métodos: A diabetes tipo 1 foi induzida através de injeção intraperitoneal de 50 mg/kg de estreptozotocina em animais. Após 42 dias de tratamento com testosterona (2mg/kg/dia) ou exercícios voluntários, individualmente ou em conjunto, as amostras de tecidos cardíacos foram coletadas e usadas para avaliação histológica e determinação de níveis de P-AKT e P-ERK através do método ELISA. Resultados: Os nossos resultados mostraram que a testosterona ou os exercícios aumentaram a capilaridade, os níveis de P-AKT, e P-ERK nos corações de ratos diabéticos. O tratamento de ratos diabéticos com testosterona e exercícios obteve um efeito sinérgico sobre a capilaridade, níveis de P-AKT, e P-ERK no coração. Além disto, na capilaridade do grupo diabético castrado, os níveis de P-AKT e P-ERK diminuíram significativamente no coração, ao passo que o tratamento com testosterona ou o treinamento com exercícios reverteu tais efeitos. O tratamento simultâneo de ratos diabéticos castrados com testosterona e exercícios obteve um efeito aditivo sobre os níveis de P-AKT e P-ERK. Conclusão: Nossas descobertas sugerem que a testosterona e exercícios, em conjunto ou individualmente, podem aumentar a angiogênese nos corações de ratos diabéticos e castrados diabéticos. Os efeitos favoráveis à angiogênese da testosterona e dos exercícios estão associados à ativação reforçada de AKT e ERK1/2 no tecido cardíaco.
Descritores: Condicionamento Físico Animal/fisiologia
Testosterona/farmacologia
MAP Quinases Reguladas por Sinal Extracelular/análise
Diabetes Mellitus Experimental/metabolismo
Coração/efeitos dos fármacos
Androgênios/farmacologia
-Fatores de Tempo
Ensaio de Imunoadsorção Enzimática
Transdução de Sinais/efeitos dos fármacos
Reprodutibilidade dos Testes
Ratos Wistar
Terapia de Reposição Hormonal/métodos
MAP Quinases Reguladas por Sinal Extracelular/efeitos dos fármacos
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Diabetes Mellitus Experimental/fisiopatologia
Diabetes Mellitus Tipo 1/fisiopatologia
Diabetes Mellitus Tipo 1/metabolismo
Coração/fisiopatologia
Androgênios/uso terapêutico
Miocárdio/química
Limites: Animais
Masculino
Tipo de Publ: Estudo de Avaliação
Responsável: BR1.1 - BIREME


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Id: lil-756699
Autor: Brito, Giovanna de.
Título: O papel da proteína prion celular na regulação da resposta à insulina / The role of cellular prion protein in the regulation of insulin signaling.
Fonte: São Paulo; s.n; 2014. 95 p. ilus, quadros.
Idioma: pt.
Tese: Apresentada a Fundação Antônio Prudente para obtenção do grau de Doutor.
Resumo: A proteína Príon Celular ou PrPc, é uma molécula de superfície celular responsável por desencadear várias cascatas de transdução de sinal e mediar muitos processos fisiológicos como proteção contra apoptose, indução da proliferação, adesão celular entre outros. Devido à sua grande gama de efeitos, hoje se acredita que PrPc seja um organizador de plataformas lipídicas, ou lipid rafts, na membrana celular. O receptor de insulina é uma proteína transmembrana também presente em plataformas lipídicas e, interessantemente, a ausência de componentes destas plataformas, como caveolinas, por exemplo, leva a uma deficiência na resposta a insulina. Desta maneira, acreditávamos que a ausência de PrPc poderia levar a uma desregulação das plataformas lipídicas e a uma sinalização ineficiente do receptor de insulina. De fato, pudemos observar a influência de PrPc no controle da glicemia sérica, através de experimentos com camundongos que fizeram ingestão de rações com conteúdo controlado de gordura. Foi possível verificar que camundongos deficientes para PrPc não possuem controle adequado da glicemia, de peso e dos níveis de insulina. Estes resultados foram confirmados em duas cepas diferentes de camundongos deficientes para PrPc. Por outro lado, camundongos que superexpressam PrPc apresentam controle adequado de glicemia por mais tempo que camundongos do tipo-selvagem quando alimentados com dietas de alta porcentagem de gordura, sugerindo que a superexpressão de PrPc promoveria uma resistência ao diabetes tipo II, com maior sensibilidade a insulina. As análises histológicas também mostraram que os animais deficientes para PrPc apresentam esteatose hepática mais acentuada do que os animais do tipo selvagem, assim como hipertrofia dos adipócitos, o que é característico de obesidade. Porém ao longo dos nossos estudos com fibroblastos derivados de camundongos deficientes para PrPc, do tipo selvagem e que superexpressam PrPc, pudemos verificar...

The cellular prion protein or PrPc is a cell surface molecule responsible for triggering various signal transduction cascades and mediate many physiological processes such as protection against apoptosis, inducing proliferation, cell adhesion, among others. Due to its wide range of effects, it is believed that PrPc is a lipid raft organizer in the cell membrane. The insulin receptor is a transmembrane protein also present in lipid rafts. Interestingly, the absence of lipid rafts's components as caveolins, for example, leads to a deficiency in insulin response. Thus, we believed that the absence of PrPc could lead to a dysregulation of lipid rafts and inefficient insulin receptor signaling. In fact, we observed the influence of PrPc in the control of serum glucose, through experiments with mice that ingested diets with controlled fat content. We found that mice deficient for PrPc do not have adequate control of blood glucose, weight gain and insulin levels. These results were confirmed in two different strains of PrPc knockout mice. On the other hand, mice overexpressing PrPc exhibit adequate control of blood glucose longer than wild-type mice when fed with high fat chow, suggesting that overexpression of PrPc promote resistance to Type II diabetes, with greater insulin sensitivity. The histological analysis also showed that PrPc deficient mice exhibit more pronounced hepatic steatosis than wild-type animals, as well as adipocyte hypertrophy, which is characteristic of obesity. However, throughout our studies with fibroblasts derived from mice deficient for PrPc, wild-type and overexpressing PrPc, we could not prove our initial hypothesis of change in insulin receptor activity. However, we observed that mice deficient for PrPc have lesser amounts of PPAR-y, a transcription factor involved in adipocyte differentiation that has influence on glucose regulation. Additionally, by flow cytometry, we found that the translocation of the glucose transporter Glut4...
Descritores: Diabetes Mellitus
Insulina
Obesidade
Proteínas PrPC
Transdução de Sinais
Limites: Humanos
Responsável: BR30.1 - Biblioteca
BR30.1


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Id: biblio-950895
Autor: Zhu, Liping; Han, Jiakai; Yuan, Rongrong; Xue, Lei; Pang, Wuyan.
Título: Berberine ameliorates diabetic nephropathy by inhibiting TLR4/NF-κB pathway
Fonte: Biol. Res;51:9, 2018. graf.
Idioma: en.
Resumo: BACKGROUND: Diabetic nephropathy (DN) is the leading cause of end-stage renal failure, contributing to severe morbidity and mortality in diabetic patients. Berberine (BBR) has been well characterized to exert renoprotective effects in DN progression. However, the action mechanism of BBR in DN remains to be fully understood. METHODS: The DN rat model was generated by intraperitoneal injection of streptozotocin (STZ, 65 mg/kg body weight) while 30 mM high glucose (HG)-treated podocytes were used as an in vitro DN model. The fasting blood glucose level and ratio of kidney weight to body weight were measured after BBR treatment (50, 100, or 200 mg/kg) in STZ-induced DN rats. The renal injury parameters including 24-h urinary protein, blood urea nitrogen and serum creatinine were assessed. qRT-PCR was performed to detect the transcript amounts of inflammatory factors. The concentrations of inflammatory factors were evaluated by ELISA kits. Western blot analysis was conducted to measure the amounts of TLR4/NF-κB-related proteins. The apoptotic rate of podocytes was analyzed by flow cytometry using Annexin V/propidium iodide. RESULTS: Berberine reduced renal injury in STZ-induced DN rat model, as evidenced by the decrease in fasting blood glucose, ratio of kidney weight to body weight, 24-h urinary protein, serum creatinine, and blood urine nitrogen. BBR attenuated the systemic and renal cortex inflammatory response and inhibited TLR4/NF-κB pathway in STZ-induced DN rats and HG-induced podocytes. Also, HG-induced apoptosis of podocytes was lowered by BBR administration. Furthermore, blockade of TLR4/NF-κB pathway by resatorvid (TAK-242) or pyrrolidine dithiocarbamate aggravated the inhibitory effect of BBR on HG-induced inflammatory response and apoptosis in podocytes. CONCLUSIONS: Berberine ameliorated DN through relieving STZ-induced renal injury, inflammatory response, and podocyte HG-induced apoptosis via inactivating TLR4/NF-κB pathway.
Descritores: Berberina/farmacologia
Transdução de Sinais/efeitos dos fármacos
NF-kappa B/antagonistas & inibidores
Diabetes Mellitus Experimental/tratamento farmacológico
Nefropatias Diabéticas/tratamento farmacológico
Receptor 4 Toll-Like/antagonistas & inibidores
-Ratos Sprague-Dawley
Limites: Animais
Masculino
Ratos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950903
Autor: Moniruzzaman, Mahammed; Ghosal, Indranath; Das, Debjit; Chakraborty, Suman Bhusan.
Título: Melatonin ameliorates H2O2-induced oxidative stress through modulation of Erk/Akt/NFkB pathway
Fonte: Biol. Res;51:17, 2018. graf.
Idioma: en.
Resumo: BACKGROUND: Improper control on reactive oxygen species (ROS) elimination process and formation of free radicals causes tissue dysfunction. Pineal hormone melatonin is considered a potent regulator of such oxidative damage in different vertebrates. Aim of the current communication is to evaluate the levels of oxidative stress and ROS induced damage, and amelioration of oxidative status through melatonin induced activation of signaling pathways. Hepatocytes were isolated from adult Labeo rohita and exposed to H2O2 at three different doses (12.5, 25 and 50 µM) to observe peroxide induced damage in fish hepatocytes. Melatonin (25, 50 and 100 µg/ml) was administered against the highest dose of H2O2. Enzymatic and non-enzymatic antioxidants such as malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) was measured spectrophotometrically. Expression level of heat shock proteins (HSP70 and HSP90), HSPs-associated signaling molecules (Akt, ERK, cytosolic and nuclear NFkB), and melatonin receptor was also measured by western blotting analysis. RESULTS: H2O2 induced oxidative stress significantly altered (P < 0.05) MDA and GSH level, SOD and CAT activity, and up regulated HSP70 and HSP90 expression in carp hepatocytes. Signaling proteins exhibited differential modulation as revealed from their expression patterns in H2O2-exposed fish hepatocytes, in comparison with control hepatocytes. Melatonin treatment of H2O2-stressed fish hepatocytes restored basal cellular oxidative status in a dose dependent manner. Melatonin was observed to be inducer of signaling process by modulation of signaling molecules and melatonin receptor. CONCLUSIONS: The results suggest that exogenous melatonin at the concentration of 100 µg/ml is required to improve oxidative status of the H2O2-stressed fish hepatocytes. In H2O2 exposed hepatocytes, melatonin modulates expression of HSP70 and HSP90 that enable the hepatocytes to become stress tolerant and survive by altering the actions of ERK, Akt, cytosolic and nuclear NFkB in the signal transduction pathways. Study also confirms that melatonin could act through melatonin receptor coupled to ERK/Akt signaling pathways. This understanding of the mechanism by which melatonin regulates oxidative status in the stressed hepatocytes may initiate the development of novel strategies for hepatic disease therapy in future.
Descritores: Transdução de Sinais/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Hepatócitos/efeitos dos fármacos
Peróxido de Hidrogênio/farmacologia
Melatonina/farmacologia
-Espectrofotometria
Superóxido Dismutase/efeitos dos fármacos
Catalase/efeitos dos fármacos
Catalase/metabolismo
Western Blotting
NF-kappa B/efeitos dos fármacos
NF-kappa B/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Hepatócitos/metabolismo
Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos
Peixes
Glutationa/efeitos dos fármacos
Glutationa/metabolismo
Malondialdeído/metabolismo
Limites: Animais
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950906
Autor: Huang, Chengchi; Lu, Hong; Xu, Junyu; Yu, Hongmin; Wang, Xiaodan; Zhang, Xiaomei.
Título: Protective roles of autophagy in retinal pigment epithelium under high glucose condition via regulating PINK1/Parkin pathway and BNIP3L
Fonte: Biol. Res;51:22, 2018. graf.
Idioma: en.
Projeto: Health and Family Planning Commission in Heilongjiang Province.
Resumo: BACKGROUND: Our study aimed to investigate the roles of autophagy against high glucose induced response in retinal pigment epithelium (ARPE-19 cells). METHODS: The morphological changes and reactive oxygen species (ROS) generation in ARPE-19 cells under high glucose treatment were respectively detected using the transmission electron microscopy and flow cytometry. The expression levels of Parkin, PINK1, BNIP3L, LC3-I and LC3-II in ARPE-19 cells received high glucose treatment were measured by western blot after pretreatment of carbonyl cyanide m-chlorophenylhydrazone (CCCP), 3-methyladenine (3-MA), N-acetyl cysteine (NAC) or cyclosporin A (CsA) followed by high glucose treatment. RESULTS: ARPE-19 cells subjected to high glucose stress showed an obvious reduction in the LC3-I expression and significant increase in the number of autophagosomes, in the intracellular ROS level, and in the expression levels of Parkin, PINK1, BNIP3L and LC3-II (p < 0.05). Pretreatment with CCCP significantly reduced the LC3-I expression and increased the expression levels of Parkin, PINK1, BNIP3L and LC3-II (p < 0.05). ARPE-19 cells pretreated with CsA under high glucose stress showed markedly down-regulated expressions of Parkin, PINK1 and BNIP3L compared with the cells treated with high glucose (p < 0.05). Pretreatment of ARPE-19 cells with NAC or 3-MA under high glucose stress resulted in a marked reduction in the expression levels of PINK1, BNIP3L and LC3-II (p < 0.05). Meanwhile, the expression level of Parkin in the ARPE-19 cells pretreated with NAC under high glucose stress was comparable with that in the control cells. CONCLUSION: Autophagy might have protective roles against high glucose induced injury in ARPE19 cells via regulating PINK1/Parkin pathway and BNIP3L.
Descritores: Proteínas Quinases/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Proteínas Proto-Oncogênicas/efeitos dos fármacos
Proteínas Supressoras de Tumor/efeitos dos fármacos
Ubiquitina-Proteína Ligases/efeitos dos fármacos
Epitélio Pigmentado da Retina/efeitos dos fármacos
Glucose/farmacologia
Proteínas de Membrana/efeitos dos fármacos
-Proteínas Quinases/metabolismo
Autofagia/fisiologia
Transdução de Sinais/fisiologia
Linhagem Celular
Proteínas Proto-Oncogênicas/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Proteínas Supressoras de Tumor/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
Microscopia Eletrônica de Transmissão
Epitélio Pigmentado da Retina/citologia
Citometria de Fluxo
Proteínas de Membrana/metabolismo
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950908
Autor: Deng, Xiuling; Wang, Dong; Wang, Shenyuan; Wang, Haisheng; Zhou, Huanmin.
Título: Identification of key genes and pathways involved in response to pain in goat and sheep by transcriptome sequencing
Fonte: Biol. Res;51:25, 2018. tab, graf.
Idioma: en.
Resumo: PURPOSE: This aim of this study was to investigate the key genes and pathways involved in the response to pain in goat and sheep by transcriptome sequencing. METHODS: Chronic pain was induced with the injection of the complete Freund's adjuvant (CFA) in sheep and goats. The animals were divided into four groups: CFA-treated sheep, control sheep, CFA-treated goat, and control goat groups (n = 3 in each group). The dorsal root ganglions of these animals were isolated and used for the construction of a cDNA library and transcriptome sequencing. Differentially expressed genes (DEGs) were identified in CFA-induced sheep and goats and gene ontology (GO) enrichment analysis was performed. RESULTS: In total, 1748 and 2441 DEGs were identified in CFA-treated goat and sheep, respectively. The DEGs identified in CFA-treated goats, such as C-C motif chemokine ligand 27 (CCL27), glutamate receptor 2 (GRIA2), and sodium voltage-gated channel alpha subunit 3 (SCN3A), were mainly enriched in GO functions associated with N-methyl-D-aspartate (NMDA) receptor, inflammatory response, and immune response. The DEGs identified in CFA-treated sheep, such as gamma-aminobutyric acid (GABA)-related DEGs (gamma-aminobutyric acid type A receptor gamma 3 subunit [GABRG3], GABRB2, and GABRB1), SCN9A, and transient receptor potential cation channel subfamily V member 1 (TRPV1), were mainly enriched in GO functions related to neuroactive ligand-receptor interaction, NMDA receptor, and defense response. CONCLUSIONS: Our data indicate that NMDA receptor, inflammatory response, and immune response as well as key DEGs such as CCL27, GRIA2, and SCN3A may regulate the process of pain response during chronic pain in goats. Neuroactive ligand-receptor interaction and NMDA receptor as well as GABA-related DEGs, SCN9A, and TRPV1 may modulate the process of response to pain in sheep. These DEGs may serve as drug targets for preventing chronic pain.
Descritores: Transdução de Sinais/genética
Dor Crônica/genética
Transcriptoma/genética
Gânglios Espinais/fisiopatologia
-Cabras
Ovinos
Transdução de Sinais/fisiologia
Biblioteca Gênica
Adjuvantes Imunológicos
Adjuvante de Freund
Limiar da Dor/fisiologia
Perfilação da Expressão Gênica
Modelos Animais de Doenças
Dor Crônica/fisiopatologia
Dor Crônica/induzido quimicamente
Transcriptoma/fisiologia
Ontologia Genética
Limites: Animais
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-1134976
Autor: Norollahi, Seyedeh Elham; Hamidian, Seyed Mohammad Taghi; Kohpar, Zeynab Khazaee; Azadi, Rezvan; Rostami, Pooya; Vahidi, Sogand; Ghazanfari, Sahar; Shabe, Farnaz Azar; Khaksar, Roya; Samadani, Ali Akbar.
Título: The fluctuation of APC gene in WNT signaling with adenine deletion of adenomatous polyposis coli, is associated in colorectal cancer / A flutuação do gene da APC na via de sinalização WNT com deleção de adenina na polipose adenomatosa do cólon está associada ao câncer colorretal
Fonte: J. coloproctol. (Rio J., Impr.);40(2):135-142, Apr.-Jun. 2020. tab, graf, ilus.
Idioma: en.
Resumo: ABSTRACT Colorectal cancer is one of the most important malignancies in the classification of gastrointestinal cancers. One of the predisposing factors at molecular level for this cancer is via WNT signaling which is associated with the vast numbers of different genes. Thus, in this study, we aimed to investigate whether Adenomatous Polyposis Coli gene (APC) mutation of rs41115in two locations such as 132.002 and 131.989 acts as a trigger or cause of colorectal cancer. Relatively, 30 blood samples of colorectal cancer patients and 30 normal blood samples as control group after colonoscopy and also confirmation of pathology report at Rohani Hospital in Babol (Iran) were investigated. The primers were designed in order to be included the rs41115 to identify the particular polymorphisms of gene. The polymerase chain reaction (PCR direct sequencing method) was used. Conclusively, deletion of adenine in two specific locations such as 131.989 and 132.002 has been identified, but there was no relationship between rs41115 polymorphisms located in adenomatous polyposis coli gene and colorectal cancer.

RESUMO O câncer colorretal é uma das neoplasias malignas mais importantes na classificação dos cânceres gastrointestinais. Um dos fatores predisponentes no âmbito molecular para esse câncer é através da via de sinalização WNT, que está associada a um grande número de genes diferentes. Portanto, neste estudo, objetivamos investigar se a mutação rs41115 do gene da polipose adenomatosa do cólon (Adenomatous Polyposis Coli - APC) em dois locais como 132.002 e 131.989 atua como gatilho ou como causa do câncer colorretal. Relativamente, 30 amostras de sangue de pacientes com câncer colorretal e 30 amostras de sangue normal (grupo controle) foram analisadas após a colonoscopia, bem como a confirmação do laudo da patologia no Rohani Hospital em Babol (Irã). Os primers foram projetados de modo a incluir o rs41115 para identificar os polimorfismos particulares do gene. A reação em cadeia da polimerase (método de sequenciamento direto por PCR) foi utilizada. Conclusivamente, a deleção de adenina em dois locais específicos, como 131.989 e 132.002, foi identificada, mas não houve relação entre o polimorfismo rs41115 localizado no gene da polipose adenomatosa do cólon e o câncer colorretal.
Descritores: Polimorfismo Genético
Neoplasias Colorretais/patologia
Genes APC
-Adenina
Transdução de Sinais/genética
Reação em Cadeia da Polimerase
Colonoscopia
Polipose Adenomatosa do Colo/patologia
Limites: Humanos
Masculino
Feminino
Responsável: BR545.3 - Biblioteca ICBS


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Id: biblio-950209
Autor: Minicucci, Marcos Ferreira; Zornoff, Leonardo Antonio Mamede.
Título: VEGFR-2: One of Pioglitazone's Signaling Pathways in the Heart / VEGFR-2: Uma das Vias de Sinalização da Pioglitazona no Coração
Fonte: Arq. bras. cardiol;111(2):170-171, Aug. 2018.
Idioma: en.
Descritores: Receptor 2 de Fatores de Crescimento do Endotélio Vascular
Tiazolidinedionas
-Transdução de Sinais
Fator A de Crescimento do Endotélio Vascular
Pioglitazona
Tipo de Publ: Comentário
Editorial
Responsável: BR1.1 - BIREME


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Id: biblio-950215
Autor: Zhong, Wenliang; Jin, Wen; Xu, Shanghua; Wu, Yanqing; Luo, Shunxiang; Liang, Minlie; Chen, Lianglong.
Título: Pioglitazone Induces Cardiomyocyte Apoptosis and Inhibits Cardiomyocyte Hypertrophy Via VEGFR-2 Signaling Pathway / Pioglitazona Induz Apoptose e Inibe Hipertrofia de Cardiomiócitos pela Via de Sinalização do VEGFR-2
Fonte: Arq. bras. cardiol;111(2):162-169, Aug. 2018. graf.
Idioma: en.
Projeto: Natural Science Foundation of Fujian Province Project.
Resumo: Abstract Background: Pioglitazone has been widely used as an insulin-sensitizing agent for improving glycemic control in patients with type 2 diabetes mellitus. However, cardiovascular risk and protective effects of pioglitazone remain controversial. Objectives: In this study, we investigated whether pioglitazone affects cardiomyocyte apoptosis and hypertrophy by regulating the VEGFR-2 signaling pathway. Methods: Cardiomyocytes were enzymatically isolated from 1- to 3-day-old Sprague-Dawley rat ventricles. Effects of pioglitazone and the VEGFR-2-selective inhibitor apatinib on cardiomyocyte apoptotic rate was determined using flow cytometry, and hypertrophy was evaluated using [3H]-leucine incorporation. The protein expressions of unphosphorylated and phosphorylated VEGFR-2, Akt, P53, and mTOR were determined by Western-Blotting. Analysis of variance (ANOVA) was used to assess the differences between groups. Results: Pioglitazone and VEGFR-2-selective inhibitor apatinib reduced rat cardiomyocyte viability and cardiomyocyte hypertrophy induced by angiotensin II in vitro. Furthermore, in the same in vitro model, pioglitazone and apatinib significantly increased the expression of Bax and phosphorylated P53 and decreased the expression of phosphorylated VEGFR-2, Akt, and mTOR, which promote cardiomyocyte hypertrophy. Conclusions: These findings indicate that pioglitazone induces cardiomyocyte apoptosis and inhibits cardiomyocyte hypertrophy by modulating the VEGFR-2 signaling pathway.

Resumo Fundamento: A pioglitazona tem sido amplamente utilizada como droga sensibilizadora da insulina para melhorar o controle glicêmico em pacientes com diabetes mellitus tipo 2. No entanto, o risco cardiovascular bem como os efeitos protetores da pioglitazona ainda são controversos. Objetivos: Neste estudo, investigamos se os efeitos da pioglitazona sobre a apoptose e a hipertrofia de cardiomiócitos ocorrem via regulação da via de sinalização do VEGFR-2. Métodos: os cardiomiócitos foram isolados enzimaticamente dos ventrículos de ratos Sprague-Dawley de 1-3 anos de vida. Os efeitos da pioglitazona e do inibidor seletivo de VEGFR-2 apatinib sobre a taxa de apoptose dos cardiomiócitos foram avaliados por citometria de fluxo, e a hipertrofia avaliada por incorporação de leucina-[3H]. As expressões de VEGFR-2, Akt, P53, e mTOR fosforiladas e não fosforiladas foram determinadas por Western Blotting. Análise de variância (ANOVA) foi usada para avaliar diferenças entre os grupos. Resultados: a pioglitazona e o apatinib reduziram a viabilidade e a hipertrofia de cardiomiócitos induzida por angiotensina II in vitro. Além disso, no mesmo modelo in vitro, a pioglitazona e o apatinib aumentaram significativamente a expressão de Bax e P53 fosforilada, e diminuiu a expressão de VEGFR-2, Akt, e mTOR, que promove hipertrofia de cardiomiócitos. Conclusões: Esses resultados indicam que a pioglitazona induz a apoptose e inibe a hipertrofia de cardiomiócitos pela modulação da via de sinalização de VEGFR-2.
Descritores: Apoptose/efeitos dos fármacos
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/efeitos dos fármacos
Tiazolidinedionas/farmacologia
Hipoglicemiantes/farmacologia
-Transdução de Sinais/efeitos dos fármacos
Ratos Sprague-Dawley
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/patologia
Pioglitazona
Hipertrofia/induzido quimicamente
Hipertrofia/patologia
Animais Recém-Nascidos
Limites: Animais
Ratos
Responsável: BR1.1 - BIREME



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