Lentivirus-mediated inhibition of tumor necrosis factor-alpha effect in expression of Caspase-3 and Bcl-2 in spinal cord contusion rats
10.3969/j.issn.1006-5725.2016.17.009
- VernacularTitle:慢病毒干扰TNF-α对脊髓损伤大鼠Caspase-3和Bcl-2表达的影响
- Author:
Yizhi WANG
;
Xi HU
;
Xiuya ZHOU
;
Hongyu XIANG
;
Ya LIN
;
Bingyi TANG
;
Tingting TANG
;
Qian ZENG
;
Xiao ZHANG
- Publication Type:Journal Article
- Keywords:
Spinal cord injury;
TNF-α;
Bcl-2;
Caspase-3
- From:
The Journal of Practical Medicine
2016;32(17):2807-2812
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the change of apoptosis factor Caspase-3 and Bcl-2 in the injured segment of rat with spinal cord injury after inhibiting lentivirus expression of inflammation factor TNF-α. To study the relationship between Caspase-3, Bcl-2, Bax and TNF-α in spinal cord injury. Mthods Spinal cord contusion model was prepared by Allen method. The relation between tumor necrosis factor alpha and Bcl-2, was predicted by the method of GeneMANIA bioinformatics. The RNA which was packaged by lentivirus constructed the RNA interference model of tumour necrosis factor alpha. After interference of tumor necrosis factor alpha, we used the method of QRT-PCR to assays the mRNA expression of Caspase-3 and Bcl-2 in spinal cord and detect of the localization of Caspase-3 and Bcl-2 by immunohistochemistry. Statistical analysis with SPSS17.0. Results SD rats had paraplegia and urinate retentaion because of spinal cord injury. The result of QRT-PCR showed that in the seventh day after SCC, the expression of Caspase-3 reduced significantly (P < 0.05) and Bcl-2 did not change significantly (P > 0.05). Immunohistochemistry experiment results showed that Caspase-3 Bcl-2 and Bax immunoreactive cells were observed in the neurons and glial cells of both white matter and gray matter in the spinal cord. The results were the same with QRT-PCR.. Conclusion TNF-α in rats after SCC can effectively regulate the ratio of Bcl-2 and Bax , and then regulate the expression of Caspase-3 , which may affect the function of apoptosis and function recovery after spinal cord injury.
