Validation experiment designed to validate causal mechanisms targeting SIRT1, FoxO3, GPX4, SLC7A11, ACSL4, FTH1, P53 in TX mice (Wilson's disease model), DL mice (control). Primary outcome: Neurological function improvement and reduction of neuronal ferroptosis
This animal model study investigated the neuroprotective mechanism of Gandouling, a Chinese medicine, in hepatolenticular degeneration (Wilson's disease) by examining its effects on the SIRT1/FoxO3 pathway-mediated ferroptosis. TX mice (disease model) were treated with various interventions including Gandouling, resveratrol (SIRT1 activator), and EX-527 (SIRT1 inhibitor) for 4 weeks. The study comprehensively evaluated neurological function through behavioral tests, assessed cellular damage markers including apoptosis and oxidative stress, and measured protein and mRNA expression of key pathway components. The research aimed to demonstrate that Gandouling protects against neuronal damage by inhibiting ferroptosis through modulation of the SIRT1/FoxO3 signaling pathway.
TX mice randomly divided into 6 groups: model control, Gandouling, resveratrol, Gandouling+resveratrol, EX-527, and Gandouling+EX-527. DL mice served as blank controls. 4-week treatment intervention followed by behavioral testing (Morris water maze, wire hanging test, pole test), TUNEL assay for apoptosis, DCFH-DA method for ROS measurement, colorimetric assays for Fe²⁺ and MDA levels, immunofluorescence for SIRT1/FoxO3, and Western blotting/qPCR for protein/mRNA expression analysis.
Gandouling treatment would improve neurological function, reduce neuronal apoptosis, decrease oxidative stress markers, and modulate SIRT1/FoxO3 pathway expression to inhibit ferroptosis
Improved performance in behavioral tests, reduced apoptosis and oxidative stress markers, and favorable modulation of SIRT1/FoxO3 pathway proteins compared to model controls
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