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1.
Protein Pept Lett ; 24(12): 1096-1104, 2018 Feb 08.
Artículo en Inglés | MEDLINE | ID: mdl-28933278

RESUMEN

BACKGROUND: Con A, a lectin extract from jackbean Canavalia ensiformis is known for its agglutination activity. ZnO nanoparticles promote the faster electron transfer between the lectin immobilized and the target cells. Hence, Con A immobilized on ZnO nanoparticles will agglutinate cells more effectively than the native protein. OBJECTIVES: Concanavalin A (Con A), a lectin was immobilized on the hexagonal zinc oxide (ZnO) nanoparticles to monitor its activity on RBCs and lymphocytes. METHODS: The immobilization of Con A and zinc oxide nanoparticles has been studied by molecular docking, microscopic and genotoxicity assessment techniques. RESULTS: Qualitative assessment using various techniques like atomic force microscopy, scanning electron microscopy and X-ray diffraction showed minor changes in morphology of Con A and ZnO nanoparticles. FT-IR spectroscopy confirmed the linking of Con A amino groups with ZnO nanoparticles. Con A immobilized nanoparticles in contrast to native lectin showed minor changes in hemagglutination activity as confirmed by pH dependence studies using fluorimetry. Con Aimmobilized nanoparticles retained the agglutination activity, this can be indicative of their potential application in detection of virus transformed and neoplastic cells. The Con A immobilized ZnO nanoparticles did not induce any significant but minor damage to whole cell DNA as revealed from comet assay or plasmid DNA. CONCLUSION: Con A immobilized on ZnO nanoparticles showed minor changes in the structure of ZnO nanoparticles and in the conformational of native Con A. However, Con A immobilized ZnO nanoparticles interestingly, showed pH resistance and better hemagglutination activity as well as minor DNA damage to whole cell lymphocytes. Thus, this novel bioaffinity support has prospective clinical implications.


Asunto(s)
Fenómenos Biofísicos , Concanavalina A/química , Concanavalina A/farmacología , Nanopartículas del Metal/química , Modelos Biológicos , Óxido de Zinc/química , Pruebas de Aglutinación/métodos , Inestabilidad Genómica/efectos de los fármacos , Hemaglutinación/efectos de los fármacos , Humanos , Microscopía de Fuerza Atómica/métodos , Simulación del Acoplamiento Molecular/métodos , Tamaño de la Partícula , Espectroscopía Infrarroja por Transformada de Fourier/métodos , Propiedades de Superficie , Difracción de Rayos X/métodos
2.
Curr Vasc Pharmacol ; 15(4): 296-312, 2017.
Artículo en Inglés | MEDLINE | ID: mdl-28155611

RESUMEN

Cells constantly adapt to external humoral cues like cytokines and hormones, but practically most cellular behavior is under locally guided control via cell-cell interactions. Galectins (Gals) are one of the most prominent members of the group of molecules involved in this intercellular signaling. They are the family of ß-galactoside specific lectins and consist of 15 different types, each with a specific function. They play crucial role in the immune system, inflammation, wound healing and carcinogenesis. In recent times, the role of Gals in the development of cardiovascular disease (CVD) has gained attention. Gals have been reported to act ambiguously by both relieving ischemia and accelerating atherosclerosis. Atherosclerosis can ultimately lead to myocardial infarction or ischemic stroke, which are both associated with Gals. There is also a role for Gals in the development of myocarditis by their influence on inflammatory processes. Moreover, Gal acts as a biomarker for the severity of myocardial ischemia and heart failure (HF). This review summarizes the association between Gals and the development and pathogenesis of CVD like atherosclerosis, stroke, myocardial infarction, and HF. A comprehensive outline of the association between Gals and more general mechanisms such as angiogenesis, arteriogenesis and atherosclerosis has also been provided. Modulation of Gal signaling holds great promise for the treatment of CVD as evident from preclinical studies.


Asunto(s)
Enfermedades Cardiovasculares/tratamiento farmacológico , Enfermedades Cardiovasculares/fisiopatología , Galectinas/efectos de los fármacos , Galectinas/fisiología , Animales , Aterosclerosis/tratamiento farmacológico , Humanos , Neovascularización Patológica/tratamiento farmacológico , Neovascularización Patológica/fisiopatología , Neovascularización Fisiológica/efectos de los fármacos
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