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Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
Cell death starts early after subarachnoid hemorrhage
Victor Friedrich1, Rowena Flores, Fatima A Sehba
1Neuroscience, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1065, New York, NY 10029, USA.
Neuroscience Letters
|February 7, 2012
Summary
Brain injury, specifically apoptosis and necrosis, begins within 10 minutes after subarachnoid hemorrhage (SAH) in rats. These findings highlight early cell death mechanisms in SAH brain injury.
Area of Science:
- Neuroscience
- Pathology
- Cell Biology
Background:
- Aneurysmal subarachnoid hemorrhage (SAH) is known to cause brain injury.
- Cell death, including apoptosis and necrosis, occurs in the brain 24 hours after SAH.
- The precise timing of the onset of cell death following SAH remains unclear.
Purpose of the Study:
- To investigate the earliest onset of cell death in the brain following SAH.
- To examine the temporal progression of apoptosis and necrosis in the brain after SAH induction.
- To identify early cellular events contributing to brain injury post-SAH.
Main Methods:
- Induction of SAH in a rat model via endovascular puncture.
- Assessment of cleaved caspase-3 (cl-caspase-3) staining at 10 minutes and 24 hours post-SAH.
- TUNEL assay to detect apoptotic cells at 10 minutes and 24 hours post-SAH.
- Fluoro-Jade staining to identify degenerating neurons at 1 hour and 24 hours post-SAH.
Main Results:
- Cl-caspase-3 positive cells (indicating apoptosis) were significantly increased in vascular and parenchymal cells at 10 minutes post-SAH compared to controls.
- TUNEL assay confirmed the presence of apoptotic cells starting at 10 minutes post-SAH, with a further increase at 24 hours.
- Fluoro-Jade positive neurons (indicating necrosis) appeared at 1 hour post-SAH and increased over time, predominantly in the ipsilateral hemisphere by 24 hours.
Conclusions:
- Apoptosis in vascular and parenchymal cells, along with neuronal necrosis, is activated very early after SAH, beginning within 10 minutes.
- These early cellular events contribute significantly to acute brain injury following SAH.
- Targeting these early cell death pathways may offer therapeutic strategies to mitigate brain damage after SAH.
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