Research Paper|Volume 15, Issue 20|pp 11546—11553

Icariin improves cognitive impairment by inhibiting ferroptosis of nerve cells

Yang Yang¹, Yiming Fu², Zhipeng Qin², Hongyan Pei³, Liping Zhai⁴, Qiaobing Guan⁴, Shasha Wu⁴, Heping Shen⁴

¹Shenyang Medical College, Shenyang 110000, Liaoning Province, China
²Criminal Investigation Police University of China, Shenyang 110000, Liaoning Province, China
³College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, Jilin, China
⁴The Second Affiliated Hospital of Jiaxing University, Jiaxing 314001, Zhejiang Province, China

Received: July 4, 2023Accepted: September 27, 2023Published: October 24, 2023

https://doi.org/10.18632/aging.205144

Copyright: © 2023 Yang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Aim: We investigated the effect and mechanism of Icariin (ICA) on improving neurobehavioral ability of mice with Alzheimer's disease (AD).

Methods: We selected 10-month-old APP/PS1 mice (AD) and wild-type C57BL/6J mice (Normal). After intragastric administration of ICA, Morris water maze was employed to detect neurobehavioral improvements, and to assay key ferroptosis indicators and oxidative stress levels. The common target of ICA for resisting ferroptosis and AD was predicted by network pharmacology.

Results: ICA could improve the neurobehavioral, memory and motor abilities of AD mice. It could lower the ferroptosis level and enhance the resistance to oxidative stress. After inhibition of MDM2, ICA could no longer improve the cognitive ability of AD mice, nor could it further inhibit ferroptosis. Network pharmacological analysis revealed that MDM2 might be the target of ICA action.

Conclusions: We found that ICA can inhibit ferroptosis of nerve cells, thereby ameliorating neural damage in mice with AD.