State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, PR China.
Department of Neurosurgery, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Changjiang Zhilu, Daping, Chongqing, 400042, PR China.
Life Sci. 2015 Jan 15;121:124-34. doi: 10.1016/j.lfs.2014.11.026. Epub 2014 Dec 9.
Previous studies in our laboratory have demonstrated the increased neuronal apoptosis in the hippocampus and abnormal hippocampal morphology after severe stress, which directly correlates to the pathogenesis of post-traumatic stress disorder (PTSD). This study aims to investigate the effects of Lycium barbarum polysaccharide (LBP) on intrusive memory of posttraumatic stress in rats, and to analyze the mechanism of regeneration/apoptosis balance in the hippocampal neurons.
The experimental rats received 20 inescapable electric foot shocks in an enclosed box for six times in three days. The rats were treated by intragastric administration of LBP (20mg/kg/day) for 3 days before stress in the stress plus prophylactic group, and for 28 days after stress in the stress plus therapeutic group. The emotion, intrusive memory-related behavior (freezing, open field, pain latency, spatial cognition), hippocampus cell morphology, and relation of neurogenesis and apoptosis in dental gyrus of the hippocampus were observed. The hippocampus volume was evaluated by stereology. Meanwhile, the neurogenesis and apoptosis were analyzed with 5-bromo-2'-deoxyuridine and terminal deoxylnucleotidyl transferase mediated-dUTP nick end labeling (TUNEL) method.
The treatment of LBP in pre-stress and post-stress had obvious beneficial effect on the behaviors and neurogenesis. The stressed rats showed improvement of intrusive memory related cognition defect, alleviation of the apoptosis in the hippocampus and recovery for the neurogenesis, which was related to the hippocampus volume after LBP treatment.
LBP treatment might effectively improve the traumatic cognition defect induced by severe stress and be useful for the intrusive memory-related cognition recovery.
本实验室之前的研究表明,严重应激后海马神经元凋亡增加和海马形态异常,这与创伤后应激障碍(PTSD)的发病机制直接相关。本研究旨在探讨枸杞多糖(LBP)对创伤后应激大鼠侵入性记忆的影响,并分析海马神经元再生/凋亡平衡的机制。
实验大鼠在封闭箱中接受 20 次不可逃避的足底电击,分 3 天进行 6 次。应激前 3 天(应激加预防组)和应激后 28 天(应激加治疗组),通过灌胃给予 LBP(20mg/kg/天)治疗。观察大鼠的情绪、与侵入性记忆相关的行为(冻结、旷场、痛觉潜伏期、空间认知)、海马细胞形态以及海马齿状回神经发生和凋亡的关系。采用体视学评估海马体积。同时,采用 5-溴-2'-脱氧尿苷和末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记(TUNEL)法分析神经发生和凋亡。
应激前和应激后给予 LBP 治疗对行为和神经发生有明显的有益作用。应激大鼠的侵入性记忆相关认知缺陷得到改善,海马细胞凋亡减轻,神经发生恢复,这与 LBP 治疗后的海马体积有关。
LBP 治疗可能有效改善严重应激引起的创伤性认知缺陷,有助于恢复与侵入性记忆相关的认知。