阿戈美拉汀改善快速动眼睡眠剥夺介导的大鼠认知功能障碍

Agomelatine improves cognitive dysfunction mediated by REM sleep deprivation in rats

目的:研究表明睡眠不足与氧化应激有关,氧化应激会导致学习和记忆障碍。褪黑素衍生物阿戈美拉汀具有抗氧化和神经保护作用。本研究探讨了阿戈美拉汀是否可以克服氧化应激,防止睡眠不足引起的认知功能障碍。方法:采用多平台模型诱导法制备大鼠快速动眼睡眠剥夺(REM-SD)模型,通过灌胃方法给予模型大鼠阿戈美拉汀。采用新物体识别实验检测大鼠空间学习记忆能力,利用商品化试剂盒检测大鼠海马组织中丙二醛(MDA)的含量和超氧化物歧化酶(SOD)的活性。结果:REM-SD严重损害了大鼠对新物体的识别能力(P<0.05),而阿戈美拉汀治疗可防止这种影响。此外,REM-SD诱导海马MDA增加,而SOD活性降低(P<0.05)。结论:REM-SD导致大鼠认知功能障碍,而阿戈美拉汀治疗可能通过使海马体中的抗氧化应激机制正常化来防止这种障碍。

Objective:Studies have linked lack of sleep to oxidative stress,which can lead to learning and memory impairments.The melatonin derivative agomelatine(AGO)has antioxidant and neuroprotective effects.This study explored whether AGO can overcome oxidative stress and prevent cognitive dysfunction caused by sleep deprivation.Methods:Rapid eye movement sleep deprivation(REM-SD)model was prepared by multi-platform model induction.AGO was administered to REM-SD rats intragastrically.The spatial learning and memory ability of rats was detected by a novel object recognition test(NOR).The content of malondialdehyde(MDA)and the activity of superoxide dismutase(SOD)in hippocampal tissue of rats were detected by commercial kits.Results:REM-SD severely impaired the ability of rats to recognize novel objects(P<0.05),and AGO treatment prevented this effect.In addition,MDA increased in hippocampus induced by REM-SD,while SOD activity decreased(P<0.05).Conclusion:REM-SD causes cognitive dysfunction in rats,and AGO treatment may prevent this impairment by normalizing the antioxidant stress mechanism in the hippocampus.