Academic Journal
Icaritin alleviates motor impairment and osteoporosis in Parkinson’s disease mice via the ER-PI3K/Akt pathway
Title: | Icaritin alleviates motor impairment and osteoporosis in Parkinson’s disease mice via the ER-PI3K/Akt pathway |
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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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ISSN: | 20452322 |
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DOI: | 10.1038/s41598-025-87429-2 |
Published in: | Scientific Reports |
Language: | English |