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Sichuan Da Xue Xue Bao Yi Xue Ban ; 45(2): 221-4, 2014 Mar.
Article in Chinese | MEDLINE | ID: mdl-24749344

ABSTRACT

OBJECTIVE: To observe the changes of apoptosis and protein kinase B/the mammalian target of Rapamycin (Akt/mTOR) signal pathway in hippocampal neurons of rat with post-straumatic stress disorder (PTSD), and to investigate the mechanism of PTSD. METHODS: Sixty male adult SD rats were divided into control group (n = 10) and PTSD (n = 50) model group. The PTSD animal model was established by giving the rats single-prolonged stress followed a single inescapable electric foot shock (SPS & S). The neuronal apoptosis of hiappocampus of PTSD rats at 1 d, 4 d, 7 d, 14 d and 28 d after model established was detected by flow cytometry (FCM). The expressions of phosphatase and tensin homology deleted on chromosome Ten (PTEN), phosphorylation of ARt and mTOR (p-Akt and p-mTOR) protein were detected by Western blotting. RESULTS: The apoptotic cell rate in PTSD 1 d, 4 d, 7 d and 14 d rats were higher than that in control rats (P < 0.05). The PTEN expression level was higher since PTSD 1 d than that in control group, and peaked in PTSD 4 d (P < 0.05). The p-Akt expression level was lower in PTSD 1 d than that in control group, and then increased in various time points after PTSD, but it was still lower in PTSD 28 d (P < 0.05). The p-mTOR expression level was lower than that in control group since PTSD 4 d, and then increased in various time points after PTSD 4 d, but it was still lower in PTSD 28 d (P < 0.05). CONCLUSION: The Akt/mTOR signal pathway was actived in hippocampal neurons of PTSD rats, and which was involved in neuronal apoptosis regulation.


Subject(s)
Apoptosis , Neurons/cytology , Proto-Oncogene Proteins c-akt/metabolism , Signal Transduction , Stress Disorders, Post-Traumatic/physiopathology , TOR Serine-Threonine Kinases/metabolism , Animals , Disease Models, Animal , Hippocampus/cytology , Male , Neurons/pathology , PTEN Phosphohydrolase/metabolism , Phosphorylation , Rats , Rats, Sprague-Dawley
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