为探究金丝桃苷在缺血再灌注损伤大鼠模型对学习记忆能力的改善及对海马组织的保护作用。本文将50只雄性SD大鼠随机分假手术组（S）、模型组（M）、金丝桃苷低（25 mg/kg）、中（50 mg/kg）、高（100 mg/kg）剂量组。除S组外，建立左侧大脑中动脉梗塞（middle cerebral artery occlusion，MCAO模型）。造模24 h后，水迷宫评估大鼠学习记忆能力；判断神经缺损；病理HE染色评价海马区神经细胞病变；免疫印迹法（western-blot）检测海马BDNF和p75NTR蛋白表达。结果表明，与M组比较，金丝桃苷能显著缩短缺血再灌注大鼠的逃避潜伏时间（15.45±1.86）s，增加穿越平台次数（8.67±1.52）次（p<0.05）；改善海马病理损伤，神经细胞形态基本正常、结构保持完整；同时调控大脑海马BDNF表达增加，p75NRT减少（p<0.05）。金丝桃苷能显著改善大鼠认知障碍，可能是通过上调BDNF、下调p75NRT减少海马神经元及细胞损伤，提高学习和记忆能力，具有一定的脑保护作用。

The brain protective effect of Lilium lancifolium hypericin on the hippocampal tissue of the rats with cerebral ischemia reperfusion injury was investigated. The 50 male SD rats were randomly divided into sham group (S), model group (M), hypericin low (25 mg/kg), middle (50 mg/kg) and high (100 mg/kg) dose groups in this work. Except S group, other groups were given the modified Longa line blockage method to establish the left middle cerebral artery occlusion (MCAO) model. After 24 hours of modeling, the learning and memory ability of rats were tested by Morris water test, and brain tissue was taken for pathological HE staining to evaluate the damage of neurons in the hippocampus. Western-blot was employed to detect the expression of BDNF and p75NTR in hippocampus. The results showed that high-dose hypericin could significantly shorten the escape latency times (15.45±1.86) and increase the number of crossing the platform (8.67±1.52) times for the ischemia-reperfusion rats, which was statistically different from that in the M group (p<0.05). In addition, the pathological damage in the hippocampal area was improved, so that the nerve cells were arranged orderly, with clear structure and basically intact and normal morphology. It can also regulate the increase of BDNF expression and the decrease of p75NRT lever in hippocampal tissue (p<0.05). Hypericin can significantly improve the cognitive impairment caused by ischemia reperfusion injury and improve the learning and memory ability. Moreover, it has a certain brain protective effect, which might be caused by the up-regulation of BDNF and down-regulation of p75NRT expressions to reduce the damage of neurons and neurons in the hippocampus.

武汉市卫计委重点项目(WX17A04)