摘要
为揭示凋亡相关基因和c-kit基因在脊髓损伤(spinal cord injury,SCI)后的相互关系,利用RT-PCR和免疫组化技术,分别检测了caspase-3、bax、bcl-2、c-kit的mRNA和蛋白在小鼠脊髓损伤后的表达。结果显示:在SCI后4 h开始出现大量的神经元和胶质细胞凋亡,其中促凋亡因子表达增加,而抑制凋亡因子表达量减少。caspase-3的mRNA和蛋白的表达在SCI后开始增加,并在72 h时达到峰值,bax表达规律与之基本一致,但是其峰值出现在24 h。随着时间的变化,bcl-2与c-kit的表达均表现为升高—降低—升高的变化趋势,与caspase-3和bax的变化趋势相反,且其调控作用均发生在caspase-3之前。此外,SCI后c-kit基因也呈现抑制凋亡的作用。表明:损伤是导致脊髓发生凋亡的因素之一;bcl-2是凋亡抑制因子,与bax共同控制细胞凋亡,并直接作用于下游caspase-3的表达。
To characterize the reciprocity mechanism of four genes in spinal cord injury （SCI） , semi-quantitative RT-PCR and im- munohistoehemistry technology were implied to investigate the expression of easpase-3, bax, bcl-2 and c-kit after SC1 in KM mouse. The results were as follows： A great of apoptosis cells were observed at 4 h after SCI, in which the expression of promoting genes increased and restraining genes reduced. The expression of caspase-3 mRNA and protein increased to peak at 72 h after SCI, and this pattern was similar to thai of bax, but the peak of bax was at 24 h. It was because trauma＇s signal stimulated 6ax firstly and then began to promote the activating of downstream target caspase-3. With the increase of time after SCI, the expression of bcl-2 and c-kit both put out increas- decrease- increase trend opposite to that of the caspase-3 and bax, and the control＇s effect happened before easpase-3. Then our research discovered that c-kit gene restrained apoptosis. It indicatted that spinal cord injury were one of important factors in apoptosis as a restraint factor, bcl-2 together with bax directly affected on the expression of downstream target caspase-3.
出处
《南京农业大学学报》
CAS
CSCD
北大核心
2010年第1期87-93,共7页
Journal of Nanjing Agricultural University
基金
科技部"十一五"国家科技支撑计划项目(2006BAD04A12)
安徽省高校省级自然科学研究重点项目(KJ2009A039)
芜湖市科技计划重点项目(2008620)
