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1.
Rev. bras. cir. cardiovasc ; 33(3): 291-302, May-June 2018. tab, graf
Article in English | LILACS | ID: biblio-958412

ABSTRACT

Abstract The heat shock proteins are endogenous proteins with the ability to act as molecular chaperones. Methods that provide cell protection by way of some damage can positively influence the results of surgery. The present review summarizes current knowledge concerning the cardioprotective role of the heat shock proteins as occurs in heart damage, including relevant information about the stresses that regulate the expression of these proteins and their potential role as biomarkers of heart disease.


Subject(s)
Humans , Myocardial Ischemia/metabolism , Myocytes, Cardiac/physiology , Cardiac Surgical Procedures , Heat-Shock Proteins/physiology , Biomarkers/metabolism , Heat-Shock Proteins/analysis , Myocardium/metabolism , Myocardium/chemistry
2.
Acta cir. bras ; 33(1): 1-13, Jan. 2018. tab, graf
Article in English | LILACS | ID: biblio-886254

ABSTRACT

Abstract Purpose: To investigate the effect of dexmedetomidine (Dex) in a rat ex vivo lung model of ischemia-reperfusion injury. Methods: An IL-2 ex vivo lung perfusion system was used to establish a rat ex vivo lung model of ischemia-reperfusion injury. Drugs were added to the perfusion solution for reperfusion. Lung injury was assessed by histopathological changes, airway pressure (Res), lung compliance (Compl), perfusion flow (Flow), pulmonary venous oxygen partial pressure (PaO2), and lung wet/dry (W/D) weight ratio. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), 78 kDa glucose-regulated protein (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP) were measured, respectively. Results: The introduction of Dex attenuated the post-ischemia-reperfusion lung damage and MDA level, improved lung histology, W/D ratio, lung injury scores and SOD activity. Decreased mRNA and protein levels of GRP78 and CHOP compared with the IR group were observed after Dex treatment. The effect of Dex was dosage-dependence and a high dose of Dex (10 nM) was shown to confer the strongest protective effect against lung damage (P<0.05). Yohimbine, an α2 receptor antagonist, significantly reversed the protective effect of Dex in lung tissues (P<0.05). Conclusion: Dex reduced ischemia-reperfusion injury in rat ex vivo lungs.


Subject(s)
Animals , Male , Reperfusion Injury/prevention & control , Dexmedetomidine/pharmacology , Adrenergic alpha-2 Receptor Agonists/pharmacology , Ischemia/prevention & control , Lung/blood supply , Reference Values , Superoxide Dismutase/analysis , Time Factors , Reperfusion Injury/pathology , Blotting, Western , Reproducibility of Results , Treatment Outcome , Rats, Sprague-Dawley , CCAAT-Enhancer-Binding Proteins/analysis , Disease Models, Animal , Real-Time Polymerase Chain Reaction , Heat-Shock Proteins/analysis , Lung/pathology , Malondialdehyde/analysis
3.
Rev. med. (Säo Paulo) ; 85(1): 3-10, 2006. ilus, tab, graf
Article in Portuguese | LILACS | ID: lil-431013

ABSTRACT

A solução hipertônica de cloreto de sódio 7,5 por cento (SSH) é eficaz em restaurar os parâmetros hemodinâmicos e reduzir a inflamação em modelos experimentais de choque hemorrágico. Assim, foi nosso objetivo investigar a ação da SSH sobre os mecanismos envolvidos na lesão de isquemia e reperfusão (I/R) em um modelo de choque hemorrágico controlado. Ratos Wistar (280-350 g) foram submetidos à hemorragia controlada, mantendo-se a pressão arterial média em 40 mmHg por 1 h / Hypertonic saline solution (HSS - NaCI 7,5 per cent) was shown to restore hemodynamic parameters in hemorrhagic shock and to decrease the inflammation triggered by ischemia-reperfusion injury (I/R). Therefore, our objective was to investigate the effects of HSS on the mechanisms involved in I/R, in an experimental model of controled hemorrhagic shock. Wistar rats (2`80-350 g) were submitted to the controled bleeding, keeping the mean arterial pressure around 40 mmHg, for 1 hour...


Subject(s)
Animals , Male , Rats , Shock/therapy , Heat-Shock Proteins/analysis , Reperfusion Injury/therapy , Neutrophil Activation , Cytokines/analysis , Oxidative Stress , Disease Models, Animal , Saline Solution, Hypertonic/therapeutic use
4.
Univ. odontol ; 24(54/55): 63-68, dic. 2004.
Article in Spanish | LILACS | ID: lil-441955

ABSTRACT

En el estudio de la respuesta inmune contra el cáncer, las proteínas de choque térmico (HSP) han sido implicadas en el control del crecimiento tumoral, al inducir una respuesta inmune en el huésped. Entre las familias de HSP que han presentado fuerte asociación con el cáncer se encuentra HSP70, la cual ha mostrado un comportamiento diferente en cada tipo de tumor. En carcinoma colorrectal y cáncer de seno, se correlacionó con baja diferenciación y pobre pronóstico. Sin embargo, alteraciones en la expresión de HSP70 en lesiones de cavidad oral han sido poco estudiadas.


Subject(s)
Humans , Heat-Shock Proteins/analysis , Mouth Neoplasms
5.
São Paulo; s.n; 2004. [195] p. tab, graf.
Thesis in Portuguese | LILACS | ID: lil-403664

ABSTRACT

A reatividade imunológica a proteínas de choque térmico 60 (Hsp60), no transplante foi descrita por vários grupos, dentre eles o nosso grupo. Estudamos a reatividade celular à Hsp60 humana, fragmentos das diferentes regiões e peptídeos desta proteína, em diferentes de camundongos sadios e em modelos de transplante através de estudo de resposta proliferativa e produção de citocinas. Também avaliamos diferentes protocolos de indução de tolerância utilizando um peptídeo derivado desta proteína. Observou-se que existe reatividade celular a diferentes regiões desta proteína em animais sadios e no modelo de transplante, com produção de citocinas pró-inflamatórias e anti-inflamatórias. Desenvolvemos um esquema de inoculação intranasal que aumentou significativamente a sobrevida do aloenxerto cardíaco. Estes resultados sugerem a manipulação da reatividade à Hsp60 poderia inibir a resposta inflamatória do enxerto e aumentar sua sobrevida / Immune reactivity to heat shock protein 60 (Hsp60) has reported in different transplantation models by different groups including our group. We studied T cell reactivity induced by recombinant human Hsp60, recombinant fragments, and peptides from this protein in three different strains of naive mice and in different murine transplantation models, analyzing T cell proliferation and cytokine production. We also developed different protocols using Hsp-peptide for tolerance induction in transplantation. We showed that both naïve and transplanted mice have Hsp60 cell reactivity with pro-inflammatory and anti-inflammatory cytokines and developed an intranasal inoculation schedule that significantly increase graft survival. These results suggest that manipulation of Hsp60 reactivity may inhibit the inflammatory response in transplantation...


Subject(s)
Transplantation Immunology/immunology , T-Lymphocyte Subsets , Autoimmunity , /analysis , Disease Models, Animal , Mice, Inbred BALB C , Heat-Shock Proteins/analysis
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