The alterations of apoptosis factor Bcl-2/Bax in the early Parkinson's disease rats and the protective effect of scorpion venom derived activity peptide / 中国应用生理学杂志
Chinese Journal of Applied Physiology
;
(6): 225-229, 2015.
Artículo
en Chino
| WPRIM
| ID: wpr-243377
ABSTRACT
<p><b>OBJECTIVE</b>To explore the alterations of apoptosis factor Bcl-2/Bax in the early Parkinson's disease (PD) rats and the protective effect of scorpion venom derived bioactive peptide.</p><p><b>METHODS</b>Healthy male SD rats (180-220 g) were randomly divided into 4 groups (n = 10) early PD model group, sham operation group, scorpion venom derived bioactive peptide control group, scorpion venom derived bioactive peptide therapy group. 6-hydroxydopamine (6-OHDA) was used to prepare the early PD rat model. The immunohistochemistry was used to detect the expression of Bax and Bcl-2 and further explore the mechanism of anti-apoptosis regarding the neuroprotective effect of scorpion venom derived bioactive peptide.</p><p><b>RESULTS</b>The results indicated that compared with the control rats, the immunostaining of Bax in the brain increased significantly while that of Bcl-2 decreased significantly in the lesion side of 6-OHDA treated rats. Interestingly, scorpion venom derived bioactive peptide could attenuate the above abnormal changes.</p><p><b>CONCLUSION</b>Up-regulation of Bax and down-regulation of Bcl-2 could participate in the early stage of PD and the anti-apoptotic mechanism could be involved in the neuroprotective effect exerted by scorpion venom derived activity peptide regarding the dopaminergic neuron in the early stage.</p>
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Enfermedad de Parkinson
/
Péptidos
/
Venenos de Escorpión
/
Regulación hacia Abajo
/
Regulación hacia Arriba
/
Química
/
Oxidopamina
/
Ratas Sprague-Dawley
/
Apoptosis
/
Fármacos Neuroprotectores
Tipo de estudio:
Estudio pronóstico
Límite:
Animales
Idioma:
Chino
Revista:
Chinese Journal of Applied Physiology
Año:
2015
Tipo del documento:
Artículo
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