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1.
Nanomedicine ; 53: 102698, 2023 09.
Artículo en Inglés | MEDLINE | ID: mdl-37507062

RESUMEN

The work aimed to investigate the biocompatibility and biological activity of the water-soluble fullerene adduct C60-Arg. It was found that the material is haemocompatible, is not cyto- and genotoxic, possesses pronounced antioxidant activity. Additionally, this paper outlines the direction of application of water-soluble fullerene adducts in the creation of neuroprotectors. It has been suggested that a putative mechanism of the protective action of the C60-Arg adduct is associated with its antioxidant properties, the ability to penetrate the blood-brain barrier, and release nitrogen monoxide as a result of the catabolism of L-arginine residues, which promote vascular relaxation. The action of the C60-Arg adduct was compared with the action of such an antioxidant as Edaravone, which is approved in Japan for the treatment of ischemic and haemorrhagic strokes.


Asunto(s)
Fulerenos , Accidente Cerebrovascular Isquémico , Nanoestructuras , Accidente Cerebrovascular , Humanos , Antioxidantes/farmacología , Antioxidantes/uso terapéutico , Fulerenos/farmacología , Fulerenos/uso terapéutico , Fulerenos/química , Agua , Accidente Cerebrovascular/tratamiento farmacológico , Isquemia , Arginina/uso terapéutico
2.
Diab Vasc Dis Res ; 15(6): 567-570, 2018 11.
Artículo en Inglés | MEDLINE | ID: mdl-30024276

RESUMEN

OBJECTIVE: Stroke is a severe complication of type 2 diabetes mellitus. Glucagon-like peptide-1 receptor agonists have been shown to have a neuroprotective effect in experimental diabetes. The aim of this study was to determine if their neuroprotective effect is an independent property of the drug independent of glycaemic control. METHODS: This two-phase study used male Wistar rats. In the first phase, experimental animals were pretreated with liraglutide, while controls received only vehicle. After transient focal brain ischaemia modelling, neurological deficit and brain infarct volume were measured. In the second phase, the first and the second groups of experimental animals with type 2 diabetes mellitus received liraglutide and metformin, respectively, while control animals with diabetes received only vehicle. After transient focal brain ischaemia modelling, neurological deficit and brain infarct volume were evaluated. RESULTS: Pretreatment with liraglutide in diabetic and non-diabetic animals reduced infarct size as compared to controls, while only non-diabetic liraglutide-treated rats presented neurologic deficit decreases. Despite glycaemia normalization, metformin-treated diabetic rats had no differences in stroke outcome when compared to the control group. CONCLUSION: The neuroprotective effect of liraglutide is not associated with glycaemic control amelioration in experimental type 2 diabetes mellitus.


Asunto(s)
Glucemia/efectos de los fármacos , Encéfalo/efectos de los fármacos , Diabetes Mellitus Experimental/tratamiento farmacológico , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Receptor del Péptido 1 Similar al Glucagón/agonistas , Hipoglucemiantes/farmacología , Ataque Isquémico Transitorio/prevención & control , Liraglutida/farmacología , Fármacos Neuroprotectores/farmacología , Animales , Glucemia/metabolismo , Encéfalo/patología , Encéfalo/fisiopatología , Diabetes Mellitus Experimental/sangre , Diabetes Mellitus Experimental/complicaciones , Diabetes Mellitus Tipo 2/sangre , Diabetes Mellitus Tipo 2/complicaciones , Receptor del Péptido 1 Similar al Glucagón/metabolismo , Ataque Isquémico Transitorio/sangre , Ataque Isquémico Transitorio/etiología , Ataque Isquémico Transitorio/patología , Masculino , Metformina/farmacología , Ratas Wistar
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