牡荆素通过调节miR-409表达逆转异氟醚诱导的神经损伤

Vitexin Reverses Isofl urane-induced Nerve damage by Regulating the Expression of miR-409

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。

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.