摘要
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基因敲除型小鼠分别分为野生型假手术组(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PCR反应法检测CDK13基因表达、TTC染色法检测脑梗死程度、免疫组化法检测脑组织中活化型半胱天冬酶-3(CC3)表达、TUNEL法检测细胞凋亡情况,四组小鼠进行相关指标比较。结果野生型模型组(MWT)小鼠脑组织梗死程度较基因敲除模型组(MKO)小鼠明显减轻(P<0.05),且脑组织凋亡阳性细胞数明显减少,凋亡指数降低,凋亡蛋白CC3表达减少(P<0.05)。结论敲除CDK13基因具有加剧小鼠缺氧性脑损伤的作用。
Objective To study the effect of CDK13 gene on apoptosis in mice with hypoxic brain injury.Methods Wild type and CDK13 knockout mice were divided into wild type sham operation group(SWT),wild type model group(MWT),gene knockout sham operation group(SKO)and gene knockout model group(MKO).The expression of CDK13 gene was detected by PCR reaction.The degree of cerebral infarction was detected by TTC staining.The expression of activated caspase-3(CC3)in brain tissue was detected by immunohistochemistry.The apoptosis was detected by TUNEL method.Four groups of mice were compared.Results Compared with the MKO group,the degree of cerebral infarction in the MWT group was significantly reduced(P<0.05),and the number of apoptotic positive cells,apoptotic index and CC3 expression were significantly decreased(P<0.05).Conclusion Knockout of CDK13 gene aggravates hypoxic brain damage in mice.
作者
王荣跃
鲁文洁
邱海凡
戴芬
WANG Rongyue;LU Wenjie;QIU Haifan;DAI Fen(Department of Obstetrics and Gynecology,the Second Affiliated Hospital of Wenzhou Medical University,Wenzhou 325000,China;Outpatient Department,the Second Affiliated Hospital of Wenzhou Medical University,Wenzhou325000,China)
出处
《中国现代医生》
2019年第34期39-42,I0002,共5页
China Modern Doctor
基金
浙江省自然科学基金项目(LY19H040006)
浙江省温州市公益性科技计划项目(Y20180491)