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Published on: December 11, 2020
Blockade of SOCE protects HT22 cells from hydrogen peroxide-induced apoptosis
1Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, PR China.
Abstract:
Oxidative stress is an established event in the pathology of neurobiological diseases. Previous studies indicated that store-operated Ca(2+) entry (SOCE) has been involved in oxidative stress. The present study was carried out to investigate the effects of SOCE inhibition on neuronal oxidative stress injury induced by hydrogen peroxide (H2O2) in HT22 cells, a murine hippocampal neuronal model. H2O2 insult induced significant intracellular Ca(2+) overload, mitochondrial dysfunction and cell viability decrease. Inhibition of SOCE by pharmacological inhibitor and STIM1 RNAi significantly alleviated intracellular Ca(2+) overload, restored the mitochondrial membrane potential (MMP), decreased cytochrome C release and eventually inhibited H2O2-induced cell apoptosis. These findings suggest that SOCE inhibition exhibited neuroprotection against oxidative stress induced by H2O2 and SOCE might be a useful therapeutic target in neurobiological disorders.
Insights
Inhibiting store-operated calcium entry (SOCE) protects neurons from oxidative stress damage caused by hydrogen peroxide (H2O2). This neuroprotection involves reducing calcium overload and improving mitochondrial function, suggesting SOCE as a therapeutic target.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Oxidative stress is implicated in neurobiological diseases.
- Store-operated calcium entry (SOCE) is linked to oxidative stress pathways.
Purpose of the Study:
- To investigate the neuroprotective effects of SOCE inhibition against hydrogen peroxide (H2O2)-induced oxidative stress in a neuronal model.
- To explore the underlying mechanisms of SOCE's role in neuronal injury.
Main Methods:
- Utilized HT22 cells, a murine hippocampal neuronal model.
- Induced oxidative stress using hydrogen peroxide (H2O2).
- Inhibited SOCE using a pharmacological inhibitor and STIM1 RNA interference (RNAi).
Main Results:
- H2O2 induced significant intracellular calcium overload, mitochondrial dysfunction, and decreased cell viability.
- SOCE inhibition alleviated calcium overload and restored mitochondrial membrane potential (MMP).
- Inhibition of SOCE reduced cytochrome C release and H2O2-induced apoptosis.
Conclusions:
- SOCE inhibition demonstrates neuroprotection against H2O2-induced oxidative stress.
- Targeting SOCE may offer a therapeutic strategy for neurobiological disorders involving oxidative stress.
