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Long-term icariin treatment ameliorates cognitive deficits via CD4+ T cell-mediated immuno-inflammatory responses in APP/PS1 mice

Authors Zhu T, Zhang F, Li H, He Y, Zhang G, Huang N, Guo M, Li X

Received 8 March 2019

Accepted for publication 15 April 2019

Published 7 May 2019 Volume 2019:14 Pages 817—826

DOI https://doi.org/10.2147/CIA.S208068

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Cristina Weinberg

Peer reviewer comments 2

Editor who approved publication: Dr Zhi-Ying Wu


Tianrui Zhu,1 Feng Zhang,1 Heng Li,1 Yi He,2 Guitao Zhang,1 Nana Huang,1 Mingming Guo,3 Xiaohong Li1

1Department of Neurology, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong 250013, People’s Republic of China; 2Department of Neurology, The Second Affiliated Hospital of Xi’an Medical University, Xi’an, Shaanxi 710021, People’s Republic of China; 3Department of Breast Surgery, The Second Hospital of Shandong University, Jinan, Shandong 250033, People’s Republic of China

Background: Alzheimer’s disease (AD) is the most common neurodegenerative disorder that also involves neuroinflammation in addition to many other features. Icariin (ICA) as one of the active ingredients of Chinese herbal medicine has the immunomodulating function. This study aimed to investigate the immunotherapeutic potential of ICA on AD.
Methods: APP/PS1 mice and wild type C57BL/6 mice were subjected to orally ICA administration (60 mg/kg/d) for 8 months. Then, the ethological and biochemical experiments, such as Morris water maze assay, Aβ ELISA, blood T cell flow cytometry, and plasma and brain cytokines array, were conducted to evaluate the effects of ICA administration.
Results: ICA significantly improved spatial learning and memory retention in APP/PS1 mice. Long-term application of ICA could also reduce hippocampus Aβ deposition, modulate the differentiation of CD4+ T cells, and modulate the release of inflammatory cytokines in plasma and brain tissue.
Conclusion: ICA shows the neuroprotective effects via modulating the CD4+ T lymphocyte-related immuno-inflammatory responses in APP/PS1 mice and may be a promising drug against AD progression.

Keywords: Alzheimer’s disease, icariin, T lymphocyte, neuroinflammation, cytokines

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