Catalpol protects synaptic proteins from beta-amyloid induced neuron injury and improves cognitive functions in aged rats

作者

Xia, ZM;Wang, FF;Zhou, S;Zhang, R;Wang, FS;Huang, JH;Wu, EX;Zhang, YF;Hu, YE

作者单位

[Xia, Zhiming; Zhang, Rui; Zhang, Yongfang; Hu, Yaer] Shanghai Jiao Tong Univ, Sch Med, Res Lab Cell Regulat, Shanghai 200025, Peoples R China.;-;[Wang, Fengfei; Zhou, Shuang; Wang, Fushun; Huang, Jason H.; Wu, Erxi] Baylor Scott & White Hlth, Dept Neurosurg, Temple, TX 76508 USA.;-;[Wang, Fengfei] Baylor Scott & White Hlth, Dept Neurol, Temple, TX 78508 USA.;-;[Wang, Fengfei; Huang, Jason H.; Wu, Erxi] Texas A&M Univ, Coll Med, Dept Surg, Temple, TX 76504 USA.;-;[Wang, Fushun] Nanjing Univ Chinese Med, Dept Psychol, Nanjing 210023, Jiangsu, Peoples R China.;-;[Wu, Erxi] Texas A&M Univ, Coll Pharm, Dept Pharmaceut Sci, College Stn, TX 77843 USA.;-;[Xia, Zhiming] Shandong Univ, Shandong Prov Hosp, Dept Nucl Med, Jinan 250021, Shandong, Peoples R China.

摘要

Synapse loss is one of the common factors contributing to cognitive disorders, such as Alzheimer's disease (AD), which is manifested by the impairment of basic cognitive functions including memory processing, perception, problem solving, and language. The current therapies for patients with cognitive disorders are mainly palliative; thus, regimens preventing and/or delaying dementia progression are urgently needed. In this study, we evaluated the effects of catalpol, isolated from traditional Chinese medicine Rehmannia glutinosa, on synaptic plasticity in aged rat models. We found that catalpol markedly improved the cognitive function of aged male Sprague-Dawley rats and simultaneously increased the expression of synaptic proteins (dynamin 1, PSD-95, and synaptophysin) in the cerebral cortex and hippocampus, respectively. In beta-amyloid (A beta) injured primary rat's cortical neuron, catalpol did not increase the viability of neuron but extended the length of microtubule-associated protein 2 (MAP-2) positive neurites and reversed the suppressive effects on expression of synaptic proteins induced by A beta. Additionally, the effects of catalpol on stimulating the growth of MAP-2 positive neurites and the expression of synaptic proteins were diminished by a PKC inhibitor, bisindolylmaleimide I, suggesting that PKC may be implicated in catalpol's function of preventing the neurodegeneration induced by A beta. Altogether, our study indicates that catalpol could be a potential disease-modifying drug for cognitive disorders such as AD.

关键词

TRIAL OBJECT RECOGNITION; ALZHEIMERS-DISEASE; A-BETA; KINASE-C; SYNAPTOPHYSIN MESSAGE; VESICLE TRAFFICKING; PREFRONTAL CORTEX; MEMORY; HIPPOCAMPUS; EXPRESSION

基本信息

所属机构:核医学

归属医师: 夏志明

PMID：29050205

UT：000411153300011

刊名:ONCOTARGET

年，卷(期):2017年8卷41期

页码：69303-69315

DOI：10.18632/oncotarget.17951

附件： pdf

收录: SCIE