ABSTRACT
Objective To study the effect of intranasal nerve growth factor (NGF) on the expression of amyloid-β,peptide (Aβ) in the central nervous system in rats with traumatic brain injury (TBI).Methods Eighty rats were randomly divided into sham(n =26),control(n =27) and treatment group (n =27 ).They were subjected to the modified Feeney' s weight-drop model.The treatment group was treated with NGF administered by nasal route,and the control group was given phosphate-buffered saline (PBS).Beam walking and Morris water maze test were performed in the three groups.The concentration of Aβ40 and Aβ42 in the injured ipsilateral hippocampus was elevated by ELISA measurement.Immunohistochemistry was used to detect the amyloid precursor protein (APP) positive cells near the region of injury in the hippocampus in rats after TBI.Results NGF group traversed the beam significantly quicker (s) than control group ( 19.00 + 6.99 vs 27.33 ± 7.39 respectively,F2,15 =12.87,P =0.028 ).Morris water maze performance revealed that mean time of latency in the NGF group was significant shorter than vehicle group,and significant memory retention in NGF group as evidenced by a greater percentage of the 60 s allotted time spent in the target quadrant (45.82％ ± 11.15％ vs 33.99％ ± 3.46％,F2,15 =6.814,P=0.037),as well as the number crossing of the former site of the removed platform in NGF group was significant more than control group (8.60 ±2.73 vs 3.60 ±2.06,F2,15 =5.346,P =0.04).The Aβ42 level in control group was increased significantly higher than NGF group as indicated by ELISA measurements.While the Aβ40 level did not have similar shown.Immunohistochemical staining showed that APP level had significant differences among three groups ( F2,15 =8.672,P =0.003).The APP level in NGF group did not alter with control group.Conclusion Intranasal administration of NGF can regulate Aβ42 overproduction,improve the motor and cognitive function after brain injury in rats.