摘要
目的探索对香豆酸(p-coumaric acid,p-CA)对急性应激小鼠记忆提取障碍的作用及其可能机制。方法采用1 h急性束缚应激(acute stress,AS)建立小鼠记忆提取障碍模型,分别运用新颖物体识别(novel object recognition,NOR)记忆提取范式和(或)物体位置识别记忆(object location recognition,OLR)提取范式检测各组小鼠记忆表现。结果NOR和OLR测试显示,与Control组相比,AS组小鼠记忆提取障碍,而p-CA可改善AS小鼠的这一现象。此外,在NOR测试中,胞外调节蛋白激酶(extracellular signal-regulated kinase,ERK)信号抑制剂PD98059和蛋白激酶A(protein kinase A,PKA)信号抑制剂H89分别阻断了p-CA对AS小鼠记忆提取的改善作用。结论p-CA改善AS诱导小鼠记忆提取障碍,并且这种作用可能依赖于ERK和PKA信号。
Aim To investigate the effect of p-coumaric acid(p-CA)on acute stress induced memory retrieval impairment in mice and its possible mechanism.Methods 1 h acute restraint stress was used to induce a model of memory retrieval impairment in mice.The memory performance of each group was detected by using the novel object recognition(NOR)memory retrieval paradigm and/or the object location recognition(OLR)memory retrieval paradigm.Results NOR and OLR tests showed that compared with control group,memory impairment was observed in AS group,which could be improved by p-CA,however.In addition,in NOR test,ERK signaling inhibitor PD98059 and PKA signaling inhibitor H89 blocked the enhancement role of p-CA in memory retrieval in AS mice.Conclusions p-CA improves AS-induced memory retrieval impairment in mice,which is dependent on ERK and PKA signaling.
作者
肖楚丽
李金成
李碧蓉
肖志勇
张文超
于旭东
XIAO Chu-li;LI Jin-cheng;LI Bi-rong;XIAO Zhi-yong;ZHANG Wen-chao;YU Xu-dong(Basic Medical School,Shaoyang University,Shaoyang Hunan 422000,China;The First Affiliated Hospital,University of South China,Hengyang Hunan 421001,China)
出处
《中国药理学通报》
CAS
CSCD
北大核心
2020年第9期1248-1253,共6页
Chinese Pharmacological Bulletin
基金
邵阳市科技计划重点项目(No 2018FJ19)
湖南省教育厅优秀青年项目(No 17B240)
湖南省自然科学基金项目(No 2019JJ50548)。
关键词
对香豆酸
急性应激
记忆提取障碍
新颖物体识别
物体位置识别
小鼠
p-coumaric acid
acute stress
memory retrieval deficit
novel objective recognition
objective location recognition
mice
