Allicin attenuates tunicamycin-induced cognitive deficits in rats via its synaptic plasticity regulatory activity.
Allicin attenuates tunicamycin-induced cognitive deficits in rats via its synaptic plasticity regulatory activity.
复制标题
大蒜素通过其突触可塑性调节活性减轻衣霉素诱导的大鼠认知缺陷。
DOI：
10.22038/ijbms.2017.8837
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发表时间：
2017-06
影响因子：
2.2
通讯作者：
Wang GC
中科院分区：
文献类型：
--
作者：
Xiang Q;Li XH;Yang B;Fang XX;Jia J;Ren J;Dong YC;Ou-Yang C;Wang GC
目的探讨大蒜素对tunicamycin （TM）所致大鼠认知功能障碍的影响及其分子机制。将200 ~ 250 g雄性SD大鼠随机分为3组：对照组（n=12）、TM组（5 μl、50 μM、ICV, n=12）和大蒜素处理组（180 mg/kg/d加饲料，n=12）。大蒜素给药16周后，以5 μl、50 μM、ICV剂量给药72 h的大鼠，采用新目标识别（NOR）测试其学习和记忆能力；细胞外电生理记录检测SC -CA1突触的场兴奋性突触后电位（fEPSP）变化，高尔基染色观察树突棘形态，Western blot检测多种突触可塑性相关蛋白。大蒜素处理组大鼠树突棘密度显著增加，认知缺陷组大鼠fEPSP对应斜率增强，海马神经元突触素和谷氨酸受体1（GluR1）表达上调。结果表明，大蒜素在突触可塑性调节中起重要作用。这些发现表明，大蒜素可以作为一种药物治疗中药诱导的认知缺陷。
To illuminate the functional effects of allicin on rats with cognitive deficits induced by tunicamycin (TM) and the molecular mechanism of this process. 200–250 g male SD rats were divided into three groups at random: control group (n=12), TM group (5 μl, 50 μM, ICV, n=12), and allicin treatment group (180 mg/kg/d with chow diet, n=12). After 16 weeks of allicin treatment, the learning ability and memory were tested using novel object recognition (NOR) testing on rats with 72 hr TM treatment (5 μl, 50 μM, ICV); meanwhile, the variation of field excitatory postsynaptic potential (fEPSP) in the Schaffer Collateral (SC)-CA1 synapse was detected by extracellular electrophysiological recordings and the morphology of dendritic spine was observed by Golgi staining as well as detecting several synaptic plasticity-related proteins by Western blot. The density of dendritic spine was increased significantly in allicin-treated groups and the correspondence slope of fEPSP in TM-induced cognitive deficits group was enhanced and expression of synaptophysin and glutamate receptor-1(GluR1) in hippocampal neurons was up-regulated. The results indicate that allicin plays an important role in synaptic plasticity regulation. These finding showed that allicin could be used as a pharmacologic treatment in TM-induced cognitive deficits.