机械加载对慢性脑缺血大鼠学习记忆障碍的改善作用

摘要：目的 探讨脉冲式机械加载对慢性脑缺血大鼠学习记忆能力的改善作用。方法 27只健康雄性SD大鼠 按随机数字表法分为假手术组（Sham组）、血管性痴呆模型组（VD组）和脊柱加载治疗组（VD+L组），每组9只。Sham 组仅分离双侧颈总动脉但不结扎；VD组分离双侧颈总动脉后永久性结扎建立VD模型；VD＋L组建立模型后每天接 受脊柱机械加载治疗，共5周。Morris水迷宫测试大鼠学习记忆能力；HE染色及尼氏染色观察大鼠大脑皮质及海马 组织的病理改变；免疫组织化学技术检测神经胶质纤维酸性蛋白（GFAP）的表达。结果 与VD组相比，VD+L组大 鼠逃避潜伏期明显缩短，穿越平台次数和停留平台象限时间显著增加，加载后明显改善神经元形态结构和存活状 态，海马锥体细胞明显增多，并抑制了海马及皮质中GFAP的表达。结论 机械加载可以明显改善慢性脑缺血后大 鼠的学习记忆障碍、保护缺血后神经元，该治疗作用可能与机械加载减轻海马和皮质神经元病理损伤、抑制胶质细 胞的活化有关。

Effects of spine loading on learning and memory impairment of chronic cerebral ischemia in rat model

Abstract: Objective To investigate the effects of spine loading on learning and memory of rats with chronic cerebral ischemia. Methods Twenty- seven healthy male SD rats were randomly divided into sham operation group (Sham group), vascular dementia model group (VD group) and spine loading treatment group (VD+L group). There were nine rats in each group. The common carotid artery was only isolated but not ligated in sham group. VD model was established by permanent occlusion of bilateral common carotid arteries in VD group. Spine loading was applied per day for 5 weeks after VD model was established in VD + L group. After loading treatment, Morris water maze was used to test the ability of learning and memory. HE staining and Nissl staining were used to observe the pathological changes of cerebral cortex and hippocampal tissues. The expression of glial fibrillary acidic protein (GFAP) was assessed by immunohistochemistry. Results Compared with the VD group, the escape latency was significantly reduced, while the number of crossing platform and staying time were significantly increased in the VD + L group. After loading, the morphological structure and survival of neurons were significantly improved, and the number of hippocampal cells increased obviously. Loading also decreased the expression of GFAP in hippocampus and cortex. Conclusion Mechanical loading significantly improves the learning and memory impairment in rats with chronic cerebral ischemia and protects neurons after ischemia. The therapeutic effect may be related with the reduced pathological damage of hippocampus and cortical neurons and the inhibited activation of glial cells