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Updated: Apr 24, 2026

Spinal Cord Neurons Isolation and Culture from Neonatal Mice
Published on: July 11, 2017
Bcl-2 in suppressing neuronal apoptosis after spinal cord injury
Ying Wang1, Zhi-Yang Sun1, Kui-Ming Zhang1
1Department of Emergency Medicine (Wang Y, Xu GQ, Li G), Department of Neurosurgery (Sun ZY, Zhang KM), Shanghai East Hospital, Shanghai, China.
Background:
Apoptosis plays an important role in central neural diseases and trauma. B-cell lymphoma/Leukemia-2 (Bcl-2) can inhibit apoptosis in a wide variety of cells including neurons. In this experiment, by studying Bcl-2 over-expression transgenic (TG) mice subjected to spinal cord injury (SCI), we investigated whether Bcl-2 could reduce posttraumatic neuronal apoptosis, reduce the range of damage, and improve the behavioral functional recovery after contusive SCI.
Methods:
Nine Bcl-2 TG mice and nine control mice were subjected to SCI of moderate severity at T10, with the use of weight dropping (WD) method (impact force 2.5×3.0 g/cm). At times up to 1 day, 7 days and 14 days after SCI, functional deficits were evaluated with Basso, Beattie, and Bresnahan (BBB) scales, and apoptosis of neurons was investigated by using the TUNEL method. Another three control mice only underwent lamina opening, but were not subjected to SCI, to provide blank comparison.
Results:
The mean functional scores for the control mice (5.05 ±0.35) were lower than those for the Bcl-2 TG mice (5.45 ±0.15), although the unpaired T-test revealed no significant difference (P=0.67). On the other hand, the number of TUNEL positive neurons and integrated option density (IOD) scores for the Bcl-2 TG mice were both significantly lower than those for the control mice (P<0.05).
Conclusions:
This experiment suggests that overexpression of Bcl-2 may suppress neuronal apoptosis after SCI. Bcl-2 may be an important factor within the central nervous system that can relieve the damage after trauma.
Insights
Overexpressing B-cell lymphoma/Leukemia-2 (Bcl-2) in mice suppressed neuronal apoptosis after spinal cord injury (SCI). This suggests Bcl-2 may be a key factor in reducing central nervous system damage from trauma.
Area of Science:
- Neuroscience
- Cell Biology
- Trauma Research
Background:
- Apoptosis is critical in central nervous system diseases and trauma.
- B-cell lymphoma/Leukemia-2 (Bcl-2) inhibits apoptosis in various cell types, including neurons.
Purpose of the Study:
- Investigate if Bcl-2 overexpression reduces neuronal apoptosis post-spinal cord injury (SCI).
- Assess Bcl-2's impact on lesion size and functional recovery after contusive SCI.
Main Methods:
- Bcl-2 transgenic (TG) mice and control littermates underwent moderate SCI using a weight-dropping method.
- Functional recovery was assessed using Basso, Beattie, and Bresnahan (BBB) scales.
- Neuronal apoptosis was quantified using the TUNEL assay.
Main Results:
- Bcl-2 TG mice showed significantly fewer TUNEL-positive neurons compared to controls (P<0.05).
- Integrated optical density (IOD) scores for apoptosis were also significantly lower in Bcl-2 TG mice.
- While mean functional scores were slightly higher in TG mice, the difference was not statistically significant (P=0.67).
Conclusions:
- Overexpression of Bcl-2 appears to suppress neuronal apoptosis following SCI.
- Bcl-2 may play a significant role in mitigating central nervous system damage after trauma.
Related Concept Videos
Secondary Spinal Cord Injury llI: Pathophysiology
Spinal Cord Injury ll: Pathophysiology
The Intrinsic Apoptotic Pathway
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