Home General Physiology and Biophysics 2025 General Physiology and Biophysics Vol.44, No.5, p. 363–375, 2025

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Founded: 1982
ISSN 1338-4325 (online)
ISSN 0231-5882 (print)
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General Physiology and Biophysics Vol.44, No.5, p. 363–375, 2025

Title: Calycosin attenuates neuronal ferroptosis in Alzheimer’s disease mice by activating the Nrf2/HO-1 pathway
Author: Qin Li, Bihua He, Ying Xiong
Abstract: In this study, we investigated the therapeutic potential of calycosin (from Astragalus) in Alzheimer’s disease (AD), focusing on ferroptosis modulation. APP/PS1 mice received 40 mg/kg calycosin for 3 months. Cognitive function was assessed via Morris water maze test. Tau hyperphosphorylation and amyloid-β (Aβ) aggregation were analyzed using immunofluorescence and Western blotting. In vitro, Aβ1-42-treated HT22 neuronal cells were exposed to calycosin. Ferroptosis-related phenotypes were assessed in vivo and in vitro using Prussian blue staining, commercial kits, and Western blotting. The nuclear factor-erythroid factor 2-related factor 2 (Nrf2) signaling was examined by Western blotting. Calycosin treatment significantly improved cognitive deficits in APP/PS1 mice and inhibited Tau hyperphosphorylation and Aβ aggregation. Calycosin attenuated neurotoxicity and Tau hyperphosphorylation in Aβ1-42-treated HT22 cells. Moreover, calycosin inhibited ferroptosis in vivo and in vitro by decreasing iron aggregation and lipid peroxidation, downregulating transferrin receptor expression, and upregulating ferroportin, cystine/glutamate antiporter, and glutathione peroxidase 4 expression. Mechanistically, the anti-ferroptosis effects of calycosin were linked to the activation of the Nrf2-mediated pathway. These findings suggest that calycosin may exhibit neuroprotective effects against neuronal ferroptosis in AD, indicating its potential as a therapeutic candidate for further investigation in AD.
Keywords: Alzheimer’s disease — Calycosin — Ferroptosis — Oxidative stress — Nrf2 — Tau protein — Amyloid-β protein
Year: 2025, Volume: 44, Issue: 5 Page From: 363, Page To: 375
doi:10.4149/gpb_2025021


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