ABSTRACT
Objective To investigate the relationship between activation of gliacytes , mitogen-activated protein kinase (p38MAPK) and neuronal apoptosis after microinjecting aggregated Aβ25-35 into hippocampus.Methods The model was established by using stereotaxic technique to inject 10μg aggregated Aβ25-35 into dorsal hippocampus in rats .The rats were grouped as the control , vehicle and model groups .Immunohistochemistry and Western blotting were used for detection of activation of microglia(MG), atrocytes (AS) and expression of p-p38MAPK in the hippocampus.ELISA was used to evaluate the level of TNF-αand IL-1β.The survival neurons were observed by Nissl staining and the apoptotic neurons were identified by tunnel staining .Results Expression of ox-42, GFAP, p-p38MAPK were up-regulated in hippocampus, as well as TNF-α、IL-1β, which reached a highest value on the 7th day after injection of Aβ25-35.However, the number of neuron with Nissl positive decreased gradually , and the tunnel positive neurons increased highly and reached a peak value on the 7th day.There were significant differences between the control and vehicle group ( P <0.01). Conclusion Apoptosis of the neuron caused by Aβ25-35 injection may result from activation of gliacytes , p38 MAPK and increase of TNF-αand IL-1βlevel.
ABSTRACT
Objective To observe changes of apoptosis and Caspase-12 expression in hippocampus of the rat model of posttraumatic stress disorder ( PTSD ) .Methods Single prolonged stress ( SPS ) was used to duplicate a rat model of PTSD.Male Wistar rats were randomly divided into 1, 4, 7 days groups after exposure to SPS and a normal control group.Transmission electron microscopy was used to observe morphologic changes of the hippocampus neurons .The expression of Caspase-12 was detected by immunohistochemistry , Western blotting and RT-PCR.Results After SPS, the hippocampus neurons had characteristic morphologic changes of apoptosis , and the expression of Caspase-12 reached the peak at SPS 4d.Conclusion PTSD activates the ERS-mediated apoptosis in hippocampus via Caspase-12, which may be a pathophysiology base of the atrophy of the hippocampus in PTSD .