Study on the role of Bcl-2 in anti- neuronal apoptosis after spinal cord injury
10.3760/cma.j.issn.1671-0282.2010.12.012
- VernacularTitle:脊髓损伤后Bcl-2抗神经元凋亡的研究
- Author:
Ying WANG
;
Zhiyang SUN
;
Kuiming ZHANG
;
Guoqiang XU
;
Guang LI
- Publication Type:Journal Article
- Keywords:
Spinal cord injury;
Tranagenic mouse;
Bcl-2;
Apoptosis of neurons
- From:
Chinese Journal of Emergency Medicine
2010;19(12):1275-1280
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the variables of behavioral function and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) figure in Bcl-2 transgenic (TG) mice and control mice after spinal cord injury (SCI), thus to find new ideas and ways for diagnosing and treating SCI. Method The genesis of Bcl-2 overexpression transgenic (TG) mice were produced by injection of Bcl-2 plasmid into the fertilized ova of mice.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). Up to 1 day , 7 days, and 14 days after SCI,functional deficits were evaluated with BBB scales, and the apoptosis of neurons was investigated by using TUNEL method. Another three mice of control group were only treated with laminectomy without SCI for comparison. Results The mean functional scores in the control mice were lower than those in the Bcl-2 TG mice, although the unpaired T -test revealed no significant differences. On the other hand, the number of TUNEL positive neurons and IOD(Integrated Optical Density)score in the Bcl-2 TG mice were both significantly lower than those in the control mice. Conclusions This experiment suggests that overexpression of Bcl-2 may suppress neuronal apoptosis after SCI. The Bcl-2 may be an important factor in relieving the damage within CNS after trauma.
