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1.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;51(1): e6858, 2018. tab, graf
Artigo em Inglês | LILACS | ID: biblio-889001

RESUMO

A novel heterometallic metal-porphyrinic framework (MPFs) built from Y and K ions as nods and meso-tetra(4-carboxyphenyl)porphyrin as linkers has been successfully synthesized and characterized. The single crystal X-ray diffraction indicated that this complex 1 exhibited a bilayered architecture of the porphyrins, which is seldom seen in MPFs. In addition, in vitro anticancer activity of complex 1 on three human breast cancer cells (BT474, SKBr-3 and ZR-75-30) was further determined.


Assuntos
Humanos , Porfirinas/química , Neoplasias da Mama/tratamento farmacológico , Estruturas Metalorgânicas/farmacologia , Estruturas Metalorgânicas/química , Antineoplásicos/farmacologia , Antineoplásicos/química , Valores de Referência , Sais de Tetrazólio , Reprodutibilidade dos Testes , Cristalografia por Raios X , Linhagem Celular Tumoral , Complexos de Coordenação/farmacologia , Complexos de Coordenação/química , Formazans
2.
Braz J Med Biol Res ; 51(1): e6858, 2017 Nov 13.
Artigo em Inglês | MEDLINE | ID: mdl-29160419

RESUMO

A novel heterometallic metal-porphyrinic framework (MPFs) built from Y and K ions as nods and meso-tetra(4-carboxyphenyl)porphyrin as linkers has been successfully synthesized and characterized. The single crystal X-ray diffraction indicated that this complex 1 exhibited a bilayered architecture of the porphyrins, which is seldom seen in MPFs. In addition, in vitro anticancer activity of complex 1 on three human breast cancer cells (BT474, SKBr-3 and ZR-75-30) was further determined.


Assuntos
Antineoplásicos/química , Antineoplásicos/farmacologia , Neoplasias da Mama/tratamento farmacológico , Estruturas Metalorgânicas/química , Estruturas Metalorgânicas/farmacologia , Porfirinas/química , Porfirinas/farmacologia , Linhagem Celular Tumoral , Complexos de Coordenação/química , Complexos de Coordenação/farmacologia , Cristalografia por Raios X , Formazans , Humanos , Ligação de Hidrogênio , Estrutura Molecular , Valores de Referência , Reprodutibilidade dos Testes , Sais de Tetrazólio
3.
Genet Mol Res ; 15(4)2016 Oct 05.
Artigo em Inglês | MEDLINE | ID: mdl-27808365

RESUMO

Neo-intima development and atherosclerosis limit the long-term use of vein grafts for revascularization of ischemic tissues. Recently, studies have confirmed that proliferating cell nuclear antigen (PCNA) plays an important role in cell proliferation. Our research confirmed that 28 days after vein transplantation, PCNA expression increases significantly. Using rabbits, rather than rodents, for a more representative model of human vein grafts, we aimed to establish a time course of changes in cell proliferation and apoptosis using morphometric and immunohistochemical analyses, western blot, terminal deoxynucleotidyl transferase dUTP nick end labeling, and transmission electron microscopy (TEM). The external jugular veins of 42 healthy purebred male New Zealand white rabbits were grafted onto their common carotid arteries. The rabbits were divided into seven groups, with vein grafts being harvested before surgery, and at 1, 3, 7, 14, 28, and 90 days afterwards. The extent of stenosis and apoptosis, PCNA protein levels, and TEM morphology were subsequently examined. Intimal thickness was slightly decreased 1 day following surgery, but then increased continuously until the 90th day. Western blot and immunohistochemistry both indicated lowered PCNA expression on day 1, although levels subsequently increased, peaking at 7 days post-surgery. After surgery, apoptosis was lowest on day 7, and remained low thereafter. TEM revealed signs of apoptosis as vein graft restenosis progressed. Proliferation and apoptosis co-occurred following grafting, indicating that both processes were involved in vein graft remodeling. Apoptosis levels were highest between days 1 and 3 after surgery, whereas proliferation culminated on the 7th day.


Assuntos
Apoptose , Prótese Vascular , Veias Jugulares/citologia , Animais , Proliferação de Células , Imuno-Histoquímica , Marcação In Situ das Extremidades Cortadas , Veias Jugulares/ultraestrutura , Masculino , Coelhos
4.
Rev. bras. ciênc. avic ; 17(n. esp): 57-64, oct.-dec. 2015. tab, graf
Artigo em Inglês | VETINDEX | ID: biblio-1490213

RESUMO

Fermented cottonseed meal (FCSM) is widely used in poultry diets in China. This study was conducted to investigate the effect of FCSM on lipid-related gene expression in broilers. Initially, 180 broiler chickens (21-days-old, equal number of males and females) were randomly divided into three groups, with six pens per group and 10 birds per pen. The chickens in the control group were fed a diet containing unfermented cottonseed meal, and those in the treatment groups were fed with diets including either CSM fermented by Candida tropicalis (Ct group) or CSM fermented by Candida tropicalis plus Saccharomyces cerevisae (Ct-Sc group) until 64 days old. The results revealed that, compared with the control group (p 0.05), the mRNA expression of peroxisome proliferator-activated receptor alpha (PPAR-a) and lipoprotein lipase (LPL) were upregulated in the livers of Ct-Sc males. The expression of PPAR-a was also upregulated in the livers of Ct females. The expression levels of acetyl CoA carboxylase (ACC) and LPL in the liver of males and the expression of PPAR-a in the liver of females were significantly different between the Ct and Ct-Sc groups (p 0.05). However, gene expressions of fatty acid synthase (FAS) and liver fatty acid-binding protein (L-FABP) in the liver were not altered when the broilers were fed FCSM-supplemented diets (p>0.05). Likewise, the expressions of peroxisome proliferator-activated receptor gamma (PPAR-g) and LPL in the abdominal fat were not altered by the FCSM-supplemented diets (p>0.05). The results in this study indicate that CSM fermented by Candida tropicalis and Saccharomyces cerevisiaeeffectively regulated the genes involved in fatty acid b-oxidation and triglyceride hydrolysis in male broiler chickens. Furthermore, the effects of the FCSM-supplemented diets were significantly different between bird sexes and between yeast strains used in the fermentation process.


Assuntos
Animais , Aves Domésticas/metabolismo , Expressão Gênica , Lipídeos/administração & dosagem , Óleo de Sementes de Algodão/administração & dosagem , Óleo de Sementes de Algodão/efeitos adversos , Leveduras
5.
R. bras. Ci. avíc. ; 17(n. esp): 57-64, oct.-dec. 2015. tab, graf
Artigo em Inglês | VETINDEX | ID: vti-17679

RESUMO

Fermented cottonseed meal (FCSM) is widely used in poultry diets in China. This study was conducted to investigate the effect of FCSM on lipid-related gene expression in broilers. Initially, 180 broiler chickens (21-days-old, equal number of males and females) were randomly divided into three groups, with six pens per group and 10 birds per pen. The chickens in the control group were fed a diet containing unfermented cottonseed meal, and those in the treatment groups were fed with diets including either CSM fermented by Candida tropicalis (Ct group) or CSM fermented by Candida tropicalis plus Saccharomyces cerevisae (Ct-Sc group) until 64 days old. The results revealed that, compared with the control group (p 0.05), the mRNA expression of peroxisome proliferator-activated receptor alpha (PPAR-a) and lipoprotein lipase (LPL) were upregulated in the livers of Ct-Sc males. The expression of PPAR-a was also upregulated in the livers of Ct females. The expression levels of acetyl CoA carboxylase (ACC) and LPL in the liver of males and the expression of PPAR-a in the liver of females were significantly different between the Ct and Ct-Sc groups (p 0.05). However, gene expressions of fatty acid synthase (FAS) and liver fatty acid-binding protein (L-FABP) in the liver were not altered when the broilers were fed FCSM-supplemented diets (p>0.05). Likewise, the expressions of peroxisome proliferator-activated receptor gamma (PPAR-g) and LPL in the abdominal fat were not altered by the FCSM-supplemented diets (p>0.05). The results in this study indicate that CSM fermented by Candida tropicalis and Saccharomyces cerevisiaeeffectively regulated the genes involved in fatty acid b-oxidation and triglyceride hydrolysis in male broiler chickens. Furthermore, the effects of the FCSM-supplemented diets were significantly different between bird sexes and between yeast strains used in the fermentation process.(AU)


Assuntos
Animais , Aves Domésticas/metabolismo , Lipídeos/administração & dosagem , Expressão Gênica , Óleo de Sementes de Algodão/administração & dosagem , Óleo de Sementes de Algodão/efeitos adversos , Leveduras
6.
Genet Mol Res ; 14(2): 3760-6, 2015 Apr 22.
Artigo em Inglês | MEDLINE | ID: mdl-25966145

RESUMO

The minimally invasive surgical transthoracic occlusion of an atrial septal defect (ASD) or a ventricular septal defect (VSD) is an increasingly widespread alternative treatment for congenital heart disease. The aim of this study is to summarize our clinical experience with minimally invasive surgical transthoracic occlusion of ASD and VSD without cardiopulmonary bypass (CPB). Between April 2011 and October 2012, 27 patients with ASD and 95 patients with VSD (78 men and 44 women) were considered for minimally invasive surgical transthoracic occlusion without CPB. A small infrasternal incision (2.0-4.0 cm) was made under general anesthesia, under transesophageal echocardiography (TEE) guidance; the ASD and VSD were closed by using an appropriate occluder; and TEE was performed simultaneously to demonstrate the position of the device, any residual shunting, or encroachment on the atrioventricular valve, coronary sinus, or aortic valve. Successful transthoracic occlusion was performed in all 122 patients without complications. No complications such as third-degree atrioventricular block and residual shunting occurred after the procedures. The ventilation time was 2.2 ± 1.2 h, and the average length of hospital stay was 4.7 ± 1.7 days. All patients received aspirin at 3 mg·kg(-1)·day(-1) (maximum 100 mg/day) 24 h after the procedure. Minimally invasive surgical transthoracic occlusion without CPB is a new treatment that has many advantages such as causing little trauma, promoting quick recovery, having less complications, and avoiding radiation damage. However, the appropriate selection of patients is still key to improving the success rate of the operation.


Assuntos
Comunicação Interatrial/cirurgia , Comunicação Interventricular/cirurgia , Adolescente , Adulto , Idoso , Procedimentos Cirúrgicos Cardíacos/métodos , Ponte Cardiopulmonar , Criança , Pré-Escolar , Feminino , Humanos , Lactente , Masculino , Pessoa de Meia-Idade , Procedimentos Cirúrgicos Minimamente Invasivos , Estudos Retrospectivos , Resultado do Tratamento , Adulto Jovem
7.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;47(5): 376-383, 02/05/2014. graf
Artigo em Inglês | LILACS | ID: lil-709439

RESUMO

The intestinal lymph pathway plays an important role in the pathogenesis of organ injury following superior mesenteric artery occlusion (SMAO) shock. We hypothesized that mesenteric lymph reperfusion (MLR) is a major cause of spleen injury after SMAO shock. To test this hypothesis, SMAO shock was induced in Wistar rats by clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h. Similarly, MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h, followed by reperfusion for 2 h. In the MLR+SMAO group rats, both the SMA and MLD were clamped and then released for reperfusion for 2 h. SMAO shock alone elicited: 1) splenic structure injury, 2) increased levels of malondialdehyde, nitric oxide (NO), intercellular adhesion molecule-1, endotoxin, lipopolysaccharide receptor (CD14), lipopolysaccharide-binding protein, and tumor necrosis factor-α, 3) enhanced activities of NO synthase and myeloperoxidase, and 4) decreased activities of superoxide dismutase and ATPase. MLR following SMAO shock further aggravated these deleterious effects. We conclude that MLR exacerbates spleen injury caused by SMAO shock, which itself is associated with oxidative stress, excessive release of NO, recruitment of polymorphonuclear neutrophils, endotoxin translocation, and enhanced inflammatory responses.


Assuntos
Animais , Masculino , Linfa/metabolismo , Oclusão Vascular Mesentérica/complicações , Traumatismo por Reperfusão/etiologia , Reperfusão/efeitos adversos , Baço/lesões , Proteínas de Fase Aguda/análise , Adenosina Trifosfatases/análise , /análise , Proteínas de Transporte/análise , Endotoxinas/análise , Molécula 1 de Adesão Intercelular/análise , Intestinos/irrigação sanguínea , Artéria Mesentérica Superior , Malondialdeído/análise , Glicoproteínas de Membrana/análise , Óxido Nítrico Sintase/análise , Óxido Nítrico/análise , Peroxidase/análise , Ratos Wistar , Baço/patologia , Superóxido Dismutase/análise , Fator de Necrose Tumoral alfa/análise
8.
Braz J Med Biol Res ; 47(5): 376-83, 2014 May.
Artigo em Inglês | MEDLINE | ID: mdl-24760116

RESUMO

The intestinal lymph pathway plays an important role in the pathogenesis of organ injury following superior mesenteric artery occlusion (SMAO) shock. We hypothesized that mesenteric lymph reperfusion (MLR) is a major cause of spleen injury after SMAO shock. To test this hypothesis, SMAO shock was induced in Wistar rats by clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h. Similarly, MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h, followed by reperfusion for 2 h. In the MLR+SMAO group rats, both the SMA and MLD were clamped and then released for reperfusion for 2 h. SMAO shock alone elicited: 1) splenic structure injury, 2) increased levels of malondialdehyde, nitric oxide (NO), intercellular adhesion molecule-1, endotoxin, lipopolysaccharide receptor (CD14), lipopolysaccharide-binding protein, and tumor necrosis factor-α, 3) enhanced activities of NO synthase and myeloperoxidase, and 4) decreased activities of superoxide dismutase and ATPase. MLR following SMAO shock further aggravated these deleterious effects. We conclude that MLR exacerbates spleen injury caused by SMAO shock, which itself is associated with oxidative stress, excessive release of NO, recruitment of polymorphonuclear neutrophils, endotoxin translocation, and enhanced inflammatory responses.


Assuntos
Linfa/metabolismo , Oclusão Vascular Mesentérica/complicações , Traumatismo por Reperfusão/etiologia , Reperfusão/efeitos adversos , Baço/lesões , Proteínas de Fase Aguda/análise , Adenosina Trifosfatases/análise , Animais , Proteínas de Transporte/análise , Endotoxinas/análise , Molécula 1 de Adesão Intercelular/análise , Intestinos/irrigação sanguínea , Receptores de Lipopolissacarídeos/análise , Masculino , Malondialdeído/análise , Glicoproteínas de Membrana/análise , Artéria Mesentérica Superior , Óxido Nítrico/análise , Óxido Nítrico Sintase/análise , Peroxidase/análise , Ratos Wistar , Baço/patologia , Superóxido Dismutase/análise , Fator de Necrose Tumoral alfa/análise
9.
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;47(1): 1-10, 01/2014. tab, graf
Artigo em Inglês | LILACS | ID: lil-697677

RESUMO

Notch signaling is an evolutionarily ancient, highly conserved pathway important for deciding cell fate, cellular development, differentiation, proliferation, apoptosis, adhesion, and epithelial-to-mesenchymal transition. Notch signaling is also critical in mammalian cardiogenesis, as mutations in this signaling pathway are linked to human congenital heart disease. Furthermore, Notch signaling can repair myocardial injury by promoting myocardial regeneration, protecting ischemic myocardium, inducing angiogenesis, and negatively regulating cardiac fibroblast-myofibroblast transformation. This review provides an update on the known roles of Notch signaling in the mammalian heart. The goal is to assist in developing strategies to influence Notch signaling and optimize myocardial injury repair.


Assuntos
Animais , Humanos , Cardiopatias/metabolismo , Miocárdio/metabolismo , Receptores Notch/metabolismo , Transdução de Sinais/fisiologia , Apoptose/fisiologia , Diferenciação Celular/fisiologia , Cardiopatias/fisiopatologia , Precondicionamento Isquêmico Miocárdico , Mamíferos , Regeneração/fisiologia
10.
Braz J Med Biol Res ; 47(1): 1-10, 2014 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-24345875

RESUMO

Notch signaling is an evolutionarily ancient, highly conserved pathway important for deciding cell fate, cellular development, differentiation, proliferation, apoptosis, adhesion, and epithelial-to-mesenchymal transition. Notch signaling is also critical in mammalian cardiogenesis, as mutations in this signaling pathway are linked to human congenital heart disease. Furthermore, Notch signaling can repair myocardial injury by promoting myocardial regeneration, protecting ischemic myocardium, inducing angiogenesis, and negatively regulating cardiac fibroblast-myofibroblast transformation. This review provides an update on the known roles of Notch signaling in the mammalian heart. The goal is to assist in developing strategies to influence Notch signaling and optimize myocardial injury repair.


Assuntos
Cardiopatias/metabolismo , Miocárdio/metabolismo , Receptores Notch/metabolismo , Transdução de Sinais/fisiologia , Animais , Apoptose/fisiologia , Diferenciação Celular/fisiologia , Cardiopatias/fisiopatologia , Humanos , Precondicionamento Isquêmico Miocárdico , Mamíferos , Regeneração/fisiologia
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