Abstract
Parkinson’s disease (PD) is a progressive neurodegenerative disorder marked by the loss of dopaminergic neurons, mitochondrial dysfunction, oxidative stress, and apoptosis. While current treatments offer symptomatic relief, they fail to halt disease progression. Early-onset PD (EOPD) is often linked to mitochondrial impairment, making it a critical target for early therapeutic intervention.This study investigates the neuroprotective effects of daidzein, a soy-derived isoflavone, against MPP⁺ (1-methyl-4-phenylpyridinum ion)-induced cytotoxicity in SH-SY5Y cells, in an in vitro model that mimics PD-related mitochondrial stress.
SH-SY5Y cells were pre-treated with daidzein (10 µM for 2 hours) before exposure to MPP⁺ (1.27 mM for 24 hours). Cell viability was assessed using the MTT assay. Oxidative stress and mitochondrial function were evaluated through thiol quantification, TBARS assay (lipid peroxidation), and TMRE staining (mitochondrial membrane potential). Dopaminergic integrity was measured using tyrosine hydroxylase (TH) ELISA.
Results showed that MPP⁺ significantly reduced cell viability, thiol levels, mitochondrial membrane potential, and tyrosine hydroxylase concentration while increasing lipid peroxidation. Pre-treatment with daidzein partially restored these parameters toward control levels, indicating its protective role against oxidative and mitochondrial damage.
In conclusion, our study showed that daidzein exhibits neuroprotective effects in a mitochondrial-dependent model of PD by attenuating oxidative stress, preserving mitochondrial function, and maintaining dopaminergic markers. These findings highlight its potential as a therapeutic candidate for EOPD.
| Date of Award | 2025 |
|---|---|
| Original language | American English |
| Supervisor | Okobi Eko Ekpo (Supervisor) |
Keywords
- Parkinson’s disease
- Daidzein
- SH-SY5Y cells
- MPP⁺
- Mitochondrial dysfunction
- Oxidative stress
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