Abstract: Objective To investigate the mechanism of vitexin in reversing isoflurane-induced nerve damage. Methods The isoflurane-induced nerve injury SD rats were constructed and divided into five groups: the model group, the vitexin low, medium, and high dose groups and the control group. Morris water maze experiment were used to evaluate the memory ability of model rats, the expression of miR-409 in hippocampus were detected by qPT-PCR, the cell apoptosis of hippocampus cells were detected by TUNEL methods. Results Vitexin could shorten the escape latency (ELP) of rats in the model group and significantly increase the expression of miR-409, inhibit apoptosis(P<0.05,P<0.01）. Conclusion Vitexin reverses the neurotoxicity induced by isoflurane by targeting miR-409 pathways.

Key words: vitexin, isoflurane, neurotoxicity, miR-409

摘要： 目的 探讨牡荆素逆转异氟醚诱导的神经损伤的作用机制。方法 用异氟醚诱导SD大鼠神经损伤模型,将大鼠随机分为五组：模型组,牡荆素低、中、高剂量组及对照组,分别采用Morris水迷宫实验评估大鼠学习记忆能力,qPT-PCR检测大鼠海马组织miR-409的表达,TUNEL法检测大鼠海马细胞凋亡情况。结果 牡荆素中、高剂量组可缩短异氟醚神经损伤大鼠的逃避潜伏期（P<0.05,P<0.01）,增加miR-409的表达（P<0.05,P<0.01）,抑制海马细胞的凋亡（P<0.05,P<0.01）。结论 牡荆素通过靶向miR-409途径逆转异氟醚诱导的神经毒性作用。

关键词: 牡荆素, 异氟醚, 神经毒性, miR-409