摘要
创伤后应激障碍(PTSD)杏仁核神经元萎缩,体积变小,存在明显的细胞凋亡现象。许多研究报道哺乳动物雷帕霉素靶蛋白(m TOR)信号通路与杏仁核神经元的凋亡有密切关系,m TOR通过调节细胞周期、蛋白质合成、细胞能量代谢等影响PTSD杏仁核细胞的调亡进程,通过靶向干预m TOR信号通路关键分子有望减缓PTSD杏仁核细胞凋亡,达到有效抗PTSD效果。
Owing to posttraumatic stress disorder (PTSD), amygdala neurons atrophy and small volume, there is obvious phenomenon of apoptosis. Many studies have reported that the mammalian target of rapamycin (mTOR) signaling pathway has a close relationship with the apoptosis of amygdala neurons, roTOR regulates apoptosis in PTSD cells through regulating cell cycle, protein synthesis, and cell energy metabolism, and PTSD signaling pathway is expected to slow down the apoptosis of PTSD cells in the mTOR signaling pathway.
出处
《台州学院学报》
2016年第3期43-46,共4页
Journal of Taizhou University
基金
浙江省科技厅公益性技术应用项目(2014C37026)