Neuroprotective effect of H2 S by inhibiting autophagy after restoration of spontaneous circulation in rats with cardiac arrest / 中国病理生理杂志
Chinese Journal of Pathophysiology
; (12): 284-289, 2016.
Artículo
en Chino
| WPRIM (Pacífico Occidental)
| ID: wpr-491588
Biblioteca responsable:
WPRO
ABSTRACT
AIM:
To investigate the neuroprotective effect of hydrogen sulfide ( H2 S) after cardiopulmonary re-suscitation in rats with cardiac arrest ( CA) , and to explore the effects of H2 S on neuron autophagy.METHODS:
The CA model was established through asphyxia.Male Wistar rats were randomly divided into sham group, model group and NaHS group.The levels of beclin-1 and LC3 II/I were measured by Western blot at 2 h, 4 h, 12 h and 24 h after the restoration of spontaneous circulation (ROSC).At 12 h after ROSC, the formation of autophagic vacuole with LC3 dots was deter-mined by immunohistochemical ( IHC) method.The phenomenon of neuron autophagy was observed under transmission electron microscope.The numbers of apoptotic neurons were counted by TUNEL staining at 72 h after ROSC.The neurolo-gic deficit score ( NDS) was used to evaluate the neurologic function after ROSC.RESULTS:
The level of beclin-1 was gradually increased in model group, but it was increased and then gradually recovered in NaHS group ( P<0.05 ) .The conversion of LC3 II in the cerebral cortex was the same as beclin-1.The results of IHC showed that LC3-positive nuclei in model group were more than those in NaHS group ( P<0.05) .The number of autophagic vacuole in model group was more than that in NaHS group (P<0.05).The number of the TUNEL-positive cells in model group was more than that in NaHS group (P<0.05).The NDS of the animals in NaHS group after ROSC was lower than that in model group(P<0.05).CONCLUSION:
H2 S inhibits neuronal autophagy, decreases apoptosis and improves neurologic function in CA rats after ROSC.
Texto completo:
Disponible
Base de datos:
WPRIM (Pacífico Occidental)
Tipo de estudio:
Estudio pronóstico
Idioma:
Chino
Revista:
Chinese Journal of Pathophysiology
Año:
2016
Tipo del documento:
Artículo