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作 者:王志芳 宁百乐 康健 方永奇[3] 李翎[3] WANG Zhi-fang;NING Bai-le;KANG Jian;FANG Yong-qi;LI Ling(Guangzhou University of Chinese Medicine,Guangzhou Guangdong,510006,China;Second Affiliated Hospital of Guangzhou University of Chinese Medicine,Guangzhou Guangdong,510120 China;First Affiliated Hospital of Guangzhou University of Chinese Medicine,Guangzhou Guangdong,510006,China)
机构地区:[1]广州中医药大学,广东广州510006 [2]广州中医药大学第二附属医院,广东广州510120 [3]广州中医药大学第一附属医院,广东广州510006
出 处:《时珍国医国药》2022年第7期1560-1563,共4页Lishizhen Medicine and Materia Medica Research
基 金:国家自然科学基金青年基金(81804166);广东省广州市科技计划项目(202102010247);广东省科技计划项目(2016A030303053);广东省中医药局中医药科研项目(20211146)。
摘 要:目的 探讨β-细辛醚对帕金森病抑郁(Depression in Parkinson’s disease,DPD)大鼠前额叶皮质自噬水平及突触可塑性的影响。方法 用6-OHDA诱导结合CUMS方法建立DPD模型大鼠并随机分组,同时设假手术组。比较假手术组、模型组、普拉克索组、帕罗西汀组、β-细辛醚低、中、高剂量组的行为学表现(OFT、PST、SPT)和纹状体α-syn的含量变化;比较假手术组、模型组、β-细辛醚中剂量组、3-MA组和雷帕霉素组大鼠前额叶皮质Beclin-1、p62和LC3I/II蛋白的表达水平和突触相关蛋白p-p70s6k、p70s6k、PSD95和synapsin 1的表达水平,观察各组大鼠神经元的形态结构。结果 β-细辛醚能改善DPD模型大鼠的运动状态、提高糖水偏好率和降低强迫游泳不动时间,减少纹状体ɑ-syn的含量,下调大鼠前额叶皮质Beclin-1和LC3I/II的表达,上调p62的表达,促进突触相关蛋白PSD95、synapsin 1、p-p70s6k和p70s6k的表达,β-细辛醚组大鼠的神经元形态结构与3-MA组相似,神经元损伤程度较轻。结论 β-细辛醚可通过抑制大鼠前额叶皮质自噬水平、调控突触可塑性,保护神经元结构,从而改善DPD模型大鼠的抑郁症状。Objective Discuss the effects of β-asarone on the prefrontal cortex autophagy level and synaptic plasticity of the rats with depression in Parkimson’s disease(DPD).Methods 6-OHDA induction and CUMS method were used to establish the DPD model rats,the rats were subject to random grouping,the sham-operated group was set,and the changes in behavioral performance(OFT,PST and SPT) and α-syn levels in corpus striatum of sham-operated group,model group,pramipexole group,paroxetine group,group with low β-asarone,group with medium β-asarone and group with high β-asarone were compared;The expression levels of Beclin-1,p62 and LC3 I/II proteins in the prefrontal cortex of rats and the expression levels of synapse-related protein p-p70 s6 k,p70 s6 k,PSD95 and synapsin 1 of sham-operated group,model group,β-asarone medium dose group,3-MA group and rapamycin group were compared and the nerve cell morphology of the rats in all groups were observed.Results The β-asarone can increase the movement distance of DPD model rats,enhance the sugar water preference rate and decrease the forced swimming immobility time,reduce the content of ɑ-syn in the corpus striatum,down-regulate the Beclin-1 and LC3 I/II expression in the prefrontal cortex of rats,up-regulate the p62 expression,and promote the expression of synapse-related protein PSD95,synapsin 1,p-p70 s6 k and p70 s6 k with the nerve cell morphology of rats in the β-asarone group being similar to that of 3-MA group,which reduced the degree of neuronal injury.Conclusion The β-asarone can regulate the synaptic plasticity by inhibiting the level of autophagy in the prefrontal cortex of rats to improve the depressive symptoms of DPD model rats.
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