Intranasal delivery of nerve growth factor attenuates neuroinflammation following traumatic brain injury in rats / 医学研究生学报
Journal of Medical Postgraduates
; (12): 1020-1022, 2014.
Article
en Zh
| WPRIM
| ID: wpr-459502
Biblioteca responsable:
WPRO
ABSTRACT
Objective Neuroinflammation following traumatic brain injury (TBI) may give rise to neurodisorder.This study aimed to investigate the effect of intranasal delivery of nerve growth factor ( NGF) on neuroinflammation following TBI and its action mechanism in rats. Methods Thirty-six male adult Sprague-Dawley rats were equally divided into a sham , a TBI, and a TBI+NGF group.The rats in the TBI +NGF group were treated with NGF intranasally at 12 and 24 hours after TBI.The levels of IL-1βand TNF-αin the injured cerebral cortex were detected by ELISA , the DNA-binding activity of NF-κB evaluated by EMSA , and the expres-sion of amyloid-β( Aβ42 ) determined by Western blot . Results NGF attenuated the inflammation following TBI .Compared with the TBI group, the level of IL-1βwas obviously decreased in the TBI +NGF group at 12 hours (70.65 ±3.10 vs 37.51 ±1.92) and 24 hours (68.85 ±8.10 vs 36.23 ±2.99, P<0.05), and so was that of TNF-α(47.12 ±7.38 vs 27.63 ±5.77 and 56.15 ±11.20 vs 29.94 ±8.62, P<0.05).The DNA-binding activity of NF-κB was reduced to 111.62 ±0.49 and 131.52 ±0.88, and the expression of Aβ42 to 0.23 ±0.008 and 0.52 ±0.004 at 12 and 24 hours respectively after treatment with NGF , both with statistically significant differences from the TBI group (P<0.05). Conclusion Intranasal administration of NGF attenuates TBI-induced neuroinflamma-tion in rats, which may be associated with its regulatory effect on the Aβ42/NF-κB signaling pathway .
Texto completo:
1
Base de datos:
WPRIM
Idioma:
Zh
Revista:
Journal of Medical Postgraduates
Año:
2014
Tipo del documento:
Article