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SUI Zhu-xin, LIU Hao, WANG Hai-tao. et al. Alteration of Apoptosis and Akt/mTOR Signal Pathway in Hippocampal Neurons of Rat with Post-traumatic[J]. Journal of Sichuan University (Medical Sciences), 2014, 45(2): 221-224.
Citation: SUI Zhu-xin, LIU Hao, WANG Hai-tao. et al. Alteration of Apoptosis and Akt/mTOR Signal Pathway in Hippocampal Neurons of Rat with Post-traumatic[J]. Journal of Sichuan University (Medical Sciences), 2014, 45(2): 221-224.

Alteration of Apoptosis and Akt/mTOR Signal Pathway in Hippocampal Neurons of Rat with Post-traumatic

  • 【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.
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