Icaritin alleviates motor impairment and osteoporosis in Parkinson’s disease mice via the ER-PI3K/Akt pathway

Bibliographic Details
Title: Icaritin alleviates motor impairment and osteoporosis in Parkinson’s disease mice via the ER-PI3K/Akt pathway
Authors: Xianmei Lin, Xinyu Zhou, Xingman Liu, Lingqiong Xia, Jing Cai, Nanqu Huang, Yong Luo, Weidong Wu
Source: Scientific Reports, Vol 15, Iss 1, Pp 1-12 (2025)
Publisher Information: Nature Portfolio, 2025.
Publication Year: 2025
Collection: LCC:Medicine
LCC:Science
Subject Terms: Parkinson’s disease, Icaritin, Estrogen receptor, Postmenopausal women, Phosphatidylinositol 3-kinase, Protein kinase B, Medicine, Science
More Details: Abstract This study investigates the role of flavonoid Icaritin (ICT) in estrogen-deficient ovariectomized (OVX) female mice by activating the Estrogen receptor (ER)/ Phosphatidylinositol 3-kinase (PI3K)/Protein kinase B (Akt) signaling pathway, potentially delaying Parkinson’s disease (PD) progression post-castration. Seventy-five 8-week-old C57BL/6J female mice underwent ovariectomy, followed by MPTP (20 mg/kg) injection for 7 days. ICT (20 mg/kg) was administered for 14 days, and motor function was assessed using various behavioral tests. Serum estradiol, FSH, LH levels were measured by ELISA, and the expression of PI3K/Akt signaling and apoptosis proteins was analyzed by Western blot. Bone mineral density was assessed via dual-energy X-ray absorption, and histology of the uterus and femur was performed. Results showed that ICT alleviated MPTP-induced motor deficits, increased serum estradiol, and improved uterine atrophy. At the molecular level, ICT activated the PI3K/Akt pathway, reduced apoptosis, and mitigated PD symptoms and osteoporosis induced by OVX. These findings suggest ICT may offer therapeutic potential in managing OVX-induced motor dysfunction and PD.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2045-2322
Relation: https://doaj.org/toc/2045-2322
DOI: 10.1038/s41598-025-87429-2
Access URL: https://doaj.org/article/6d4d7f0ee8dd4340ab3ae2fe6b5a2939
Accession Number: edsdoj.6d4d7f0ee8dd4340ab3ae2fe6b5a2939
Database: Directory of Open Access Journals
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More Details
ISSN:20452322
DOI:10.1038/s41598-025-87429-2
Published in:Scientific Reports
Language:English