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Glial high-mobility group box 1 translocation promotes post-stroke epileptic seizures
Chao Zhong1, Wenqi Wang1, Jinghong Li1
1Zhejiang Collaborative Innovation Center for the Brain Diseases with Integrative Medicine, Zhejiang Key Laboratory of Neuropsychopharmacology, School of Pharmaceutical Sciences, & First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
High mobility group box 1 (HMGB1) translocation in glial cells drives post-stroke epilepsy (PSE). Anti-HMGB1 antibody therapy effectively suppresses seizures and cognitive deficits in PSE models, offering a promising treatment strategy.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Post-stroke epilepsy (PSE) is a frequent and treatment-resistant complication following ischemic stroke.
- The precise mechanisms underlying PSE development and progression remain incompletely understood.
- High mobility group box 1 (HMGB1) is implicated in various neurological conditions, but its role in PSE is not well-defined.
Purpose of the Study:
- To investigate the role of HMGB1 in the pathogenesis of post-stroke epilepsy (PSE).
- To evaluate the therapeutic potential of anti-HMGB1 monoclonal antibody treatment for PSE.
- To elucidate the cellular mechanisms underlying HMGB1's contribution to seizure susceptibility after stroke.
Main Methods:
- Utilized a photothrombotic stroke model in mice to induce ischemic injury and assess seizure susceptibility.
- Quantified nuclear-to-cytoplasmic translocation of HMGB1 in neuronal and glial cells.
- Administered an anti-HMGB1 monoclonal antibody to PSE model mice and evaluated seizure frequency, seizure susceptibility, and cognitive function.
Main Results:
- Extensive cortical lesions following ischemic stroke significantly enhanced seizure susceptibility in mice.
- HMGB1 nuclear-to-cytoplasmic translocation, particularly in glial cells, correlated positively with seizure severity.
- Anti-HMGB1 antibody treatment suppressed spontaneous seizures, reduced pentylenetetrazol-induced seizure susceptibility, and improved cognitive deficits.
- Therapeutic effects were associated with reduced glial activation and inhibited HMGB1 translocation.
Conclusions:
- Glial HMGB1 translocation is identified as a critical mediator of post-stroke epilepsy (PSE) pathogenesis.
- Targeting HMGB1 with monoclonal antibody therapy demonstrates significant neuroprotective effects and seizure suppression in PSE models.
- Anti-HMGB1 therapy represents a promising novel therapeutic strategy for managing post-stroke epilepsy and associated cognitive impairments.
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