CDK13基因对缺氧性脑损伤小鼠细胞凋亡的影响

Effects of CDK13 gene on cell apoptosis in neonatal mice with hypoxic brain damage

目的研究CDK13基因对缺氧性脑损伤小鼠细胞凋亡的影响。方法将野生型和CDK13基因敲除型小鼠分为野生型假手术组别(SWT)、野生型模型组(MWT)、基因敲除假手术组(SKO)及基因敲除模型组(MKO)。采用TTC染色法检测各组新生小鼠脑梗死程度;采用免疫组化法检测脑组织中活化型半胱天冬酶-3(CC3)的表达;TUNEL法检测细胞凋亡情况。结果野生型模型组(MWT)组小鼠脑组织梗死程度较基因敲除模型组(MKO)组小鼠明显减轻(P<0.05);并且脑组织凋亡阳性细胞数明显减少,凋亡指数降低(P<0.05);凋亡蛋白CC3表达减少(P<0.05)。结论敲除CDK13基因对新生鼠缺氧性脑损伤具有加剧作用。

Objective:To study the effect of CDK13(Cyclin-dependent kinases 13)gene on cell apoptosis in neonatal mice with hypoxic brain damage.Methods:Wild type C57BL/6 mice and CDK13 gene knockout neonatal C57BL/6 mice were randomly divided into four groups:sham-operated wild-type(SWT),MCAO model wild type(MWT),sham-operated knockout(SKO)and MCAO model knockout(MKO).TTC(2,3,5-triphenyl four azole nitrogen chloride)staining was used to measure brain infarct volume.The expression of cleaved caspase-3(CC3)was peformed on brain tissues.Cell apoptosis was performed by the TUNEL method.Results:Compared with the MKO group,the infarct volume of brain tissues was reduced in the MWT group(P<0.05),the number of apoptotic cells was decreased in the MKO group,the apoptosis protein CC3 was significantly reduced in the MKO group.Conclusion:Cdk13 gene knockout can increase the death neonatal MCAO mice.