Research Papers: Gerotarget (Focus on Aging):
Catalpol protects synaptic proteins from beta-amyloid induced neuron injury and improves cognitive functions in aged rats
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Zhiming Xia1,7,*, Fengfei Wang2,3,4,*, Shuang Zhou2,*, Rui Zhang1, Fushun Wang2,5, Jason H. Huang2,4, Erxi Wu2,4,6, Yongfang Zhang1, Yaer Hu1
1 Research Laboratory of Cell Regulation, School of Medicine, Shanghai Jiaotong University, Shanghai 200025, China
2 Department of Neurosurgery, Baylor Scott & White Health, Temple, Texas 76508, USA
3 Department of Neurology, Baylor Scott & White Health, Temple, Texas 78508, USA
4 Department of Surgery, Texas A & M University College of Medicine, Temple, Texas 76504, USA
5 Department of Psychology, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, China
6 Department of Pharmaceutical Sciences, Texas A & M University College of Pharmacy, College Station, Texas 77843, USA
7 Current address: Department of Nuclear Medicine, Shandong Provincial Hospital, Shandong University, Jinan, Shandong 250021, China
* Equal first author
Erxi Wu, email:
Yongfang Zhang, email:
Yaer Hu, email:
Keywords: catalpol, synaptic proteins, neuron injury, cognitive functions, Alzheimer’s disease, Gerotarget
Received: November 24, 2016 Accepted: March 30, 2017 Published: May 17, 2017
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 (Aβ) 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 Aβ. 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 Aβ. Altogether, our study indicates that catalpol could be a potential disease-modifying drug for cognitive disorders such as AD.
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