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Updated: Jun 26, 2026
Monitoring Astrocyte Reactivity and Proliferation in Vitro Under Ischemic-Like Conditions
Published on: October 21, 2017
Mitochondrial dysfunction of Astrocyte induces cell activation under high salt condition
Yuemin Qiu1,2, Gengxin Lu1, Shifeng Zhang1
1Department of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
High salt intake disrupts astrocyte mitochondrial function, impacting brain health. Targeting translocator protein (TSPO) signaling may offer a therapeutic strategy against high-salt neurotoxicity.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Excess dietary sodium accumulation in the brain negatively impacts health.
- High salt intake activates astrocytes, leading to the secretion of inflammatory factors.
Purpose of the Study:
- To investigate the effects of high salt on astrocyte internal cell metabolism.
- To explore the role of mitochondrial function in high-salt-induced astrocyte activation.
Main Methods:
- RNA sequencing to analyze astrocyte gene expression under high salt conditions.
- High Intelligent and Sensitive Structured Illumination Microscopy (HIS-SIM) to observe mitochondrial morphology.
- Measurement of mitochondrial oxygen consumption and membrane potential.
Main Results:
- High salt downregulated oxidative phosphorylation and glycolysis pathways in astrocytes.
- High salt caused astrocyte mitochondria to swell and change shape.
- High salt reduced mitochondrial oxygen consumption and membrane potential.
- Treatment with 18-kDa translocator protein (TSPO) ligand FGIN-1-27 improved mitochondrial networks and reversed astrocyte activation.
Conclusions:
- High salt directly disrupts astrocytic mitochondrial homeostasis and function.
- Targeting translocator protein (TSPO) signaling presents a potential therapeutic approach for high-salt neurotoxicity.
