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Spermidine ameliorates the neuronal aging by improving the mitochondrial function in vitro.
Yu-Hong Jing1, Ji-Long Yan2, Qing-Jun Wang2
1Institute of Anatomy and Histology & Embryology, Neuroscience, School of Basic Medical Sciences, Lanzhou University, No. 199 of Donggang West Road, Lanzhou City, Gansu province 730000, PR China; Key Laboratory of Preclinical Study for New Drugs of Gansu Province, Lanzhou University, No. 199 of Donggang West Road, Lanzhou City, Gansu province 730000, PR China.
Experimental Gerontology
|April 13, 2018
Summary
Spermidine delays neuronal cell aging by preserving mitochondrial function and stability. This natural compound maintains mitochondrial membrane potential and oxygen utilization, counteracting age-related decline.
Area of Science:
- Cellular and Molecular Biology
- Neuroscience
- Aging Research
Background:
- Mitochondrial dysfunction is a key driver of cellular aging.
- Spermidine exhibits anti-aging properties, but its impact on neuronal aging and mitochondrial mechanisms requires further investigation.
Purpose of the Study:
- To investigate the anti-aging effects and underlying mechanisms of spermidine in a mouse neuroblastoma (N2a) cell model of aging.
- To determine if spermidine can protect against d-galactose-induced neuronal cell aging and mitochondrial damage.
Main Methods:
- Established cell aging in N2a cells using d-galactose (d-Gal) treatment.
- Assessed cell cycle, β-galactosidase activity, mitochondrial mRNA stability, and mitochondrial membrane potential (MMP).
- Utilized Seahorse Metabolic Analysis for mitochondrial function, ATP production, and analyzed the unfolded protein response (UPR).
Main Results:
- Spermidine pretreatment delayed d-Gal-induced cell aging, increased cells in S phase, and maintained MMP.
- d-Gal reduced oxygen utilization and ATP production, which were partially restored by spermidine.
- Spermidine promoted autophagy and inhibited apoptosis, except for the UPR, ameliorating N2a cell aging.
Conclusions:
- Spermidine effectively ameliorates neuronal cell aging by maintaining mitochondrial mRNA transcription, MMP, and oxygen utilization.
- Spermidine's protective effects involve preserving mitochondrial stability and function during aging processes.
- The findings highlight spermidine as a potential therapeutic agent for age-related neuronal decline.
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