缺氧对耳蜗听神经元电压门控性钠通道及凋亡因子表达的影响  

Regulation on voltage gated sodium channels and Caspase-3 expression in spiral ganglion neurons by hypoxia

作　　者：冯爽 陈敬伟 黄振云 邵剑波 罗仁忠 FENG Shuang;CHEN Jingwei;HUANG Zhenyun;SHAO Jianbo;LUO Renzhong(Department of Otolaryngology,Guangzhou Women and Children′s Medical Center,Guangzhou,Guangdong 510120,China)

机构地区：[1]广州市妇女儿童医疗中心耳鼻咽喉科

出　　处：《现代医药卫生》2019年第11期1616-1618,共3页Journal of Modern Medicine & Health

基　　金：广东省科技厅科技计划项目(2014A020212019);广州市卫生健康委员会医药卫生科技项目(20141A011026,20151A011023)

摘　　要：目的研究缺氧对大鼠螺旋神经节神经元(SGN)电压门控性钠通道及凋亡因子表达水平的影响。方法分离出生3dSD大鼠SGN并进行原代培养,对照组给予常规培养处理,实验组给予无氧培养处理24h,提取总RNA,采用荧光定量聚合酶链反应(qPCR)检测凋亡因子Caspase-3,电压门控性钠通道Nav1.1、Nav1.6及Nav1.7α亚单位mRNA表达水平,比较实验组和对照组各基因mRNA表达水平。结果与对照组相比,实验组大鼠SGN Caspase-3、Nav1.1和Nav1.7α亚单位mRNA表达上调,Nav1.6α亚单位mRNA表达下调(P<0.05)。结论缺氧可能促进Caspase介导的SGN凋亡过程,并调控电压门控性钠通道的表达,该调控作用具有亚型选择性特点,可能是缺氧引起听力下降的机制之一。Objective To investigate the effect of hypoxia on the expression of voltage gated sodium channels and apoptotic factors in spiral ganglion neurons(SGN). Methods The expression of Nav1.1,Nav1.6 and Nav1.7 α subunit mRNA in SGN were detected by using quantitative polymerase chain reaction(qPCR),after cultured under tradition condition or hypoxia condition.The mRNA level of Caspase-3 was also investigated by using qPCR. Results Hypoxia exposure for 24 h could increase the mRNA expression levels of Caspase-3,Nav1.1 and Nav1.7 α subunit,and decrease the mRNA expresion level of Nav1.6 α subunit mRNA( P < 0.05 ). Conclusion Hypoxia could down-regulate the expression levevl of voltage gated sodium channels,and activate the Caspase dependent apoptotic process of SGN,which might be the mechanism of sensorineural hearing loss induce by hypoxia.

关 键 词：缺氧 电压门控性钠通道 螺旋神经节 凋亡因子 mRNA 

分 类 号：R246.81[医药卫生—针灸推拿学]