Immunohistochemical investigation of neuronal injury in cerebral cortex of cobra-envenomed rats



Título del documento: Immunohistochemical investigation of neuronal injury in cerebral cortex of cobra-envenomed rats
Revista: The journal of venomous animals and toxins including tropical diseases
Base de datos: PERIÓDICA
Número de sistema: 000298832
ISSN: 1678-9199
Autores: 1
2
Instituciones: 1Suez Channel University, Faculty of Science, Ismailia. Egipto
2United Arab Emirates University, Faculty of Science, Al-Ain. Emiratos Arabes Unidos
Año:
Volumen: 10
Número: 1
Paginación: 53-76
País: Brasil
Idioma: Inglés
Tipo de documento: Artículo
Enfoque: Experimental
Resumen en inglés The immunohistochemical expression of neuron-specific enolase, NSE (a cytoplasmic glycolytic enzyme of the neurons), synaptophysin, SYN (a major membrane glycoprotein of synaptic vesicles), and Bcl-2 (anti-apoptotic protein) were determined in cerebral cortex of rats envenomed with neurotoxic venom from Egyptian cobra. Male rats were intramuscularly (IM) injected with a single injection of either physiological saline solution or ½ LD50 or LD50 of cobra venom and sacrificed 24, 48, or 72 hr after envenoming. Formalin-fixed paraffin sections were immunohistochemically studied by avidin-biotin-peroxidase complex method. Neuron histological structure and isolation of genomic DNA were also detected. The results showed a dose and time-dependent increase in NSE and SYN immunoreactivity in cerebral cortex of envenomed rats except in 72 hr high dose envenoming, where decreased SYN was observed. On the other hand, low dose venom induced high Bcl-2 expression 24 hr after envenoming, while the high dose decreased Bcl-2 protein expression. Temporal and spatial Bcl-2 expression was accompanied by DNA fragmentation in cerebral cortex of all envenomed rats, although no serious histological alterations were noticed. These results suggest that cobra venom may lead to neuronal injury and impairment of axonal transport as ascertained by alterations in NSE and SYN immunoreactivity. It could also indicate that venom alters the molecular machinery of apoptosis by inhibiting Bcl-2 expression; however, some vulnerable cells have the ability to overcome thi
Disciplinas: Medicina
Palabras clave: Medicina experimental,
Neurología,
Toxicología,
Veneno de víbora,
Daño neuronal,
Enolasa,
Sinaptofisina,
Corteza cerebral,
Inmunohistoquímica,
Ratas
Keyword: Medicine,
Experimental medicine,
Neurology,
Toxicology,
Snake venom,
Neuronal damage,
Enolase,
Synaptophysin,
Cerebral cortex,
Immunohistochemistry,
Rats
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