反义脱氧寡核苷酸 meaning in Chinese
aodn
ason
Examples
- To make clear the hypothesis , a middle cerebral artery occlusion ( mcao ) and hypoxia and glucose - deprivation ( hgd ) ischemic models were used in in vivo and in vitro study , respectively . we first studied the cellular localization of kvl . 2 and the co - localization of kvl . 2 protein and vegf receptors flk - 1 and flt - 1 , observed the effect of mcao on kvl . 2 expression and phosphrylation in the rat brain in vivo , then investigated the effect of vegf on ischemia / hypoxia cell damage and tyrosine phosphorylation of kvl . 2 in sh - sy5y cells . finally , in order to further elucidate the relationship between vegf ' s neuroprotection and its regulation on kvl . 2 phosphorylation , we used a specific antisense oligodeoxynucleotide ( odn ) to knockdown the expression of endogenous vegf to observe its role in ischemia / hypoxia cell damage and regulation of kvl . 2 phosphorylation
为了验证上述假设，本文分别在整体和离体水平，采用大脑中动脉缺血( middlecerebralarteryocclusion ， mcao )和体外氧?糖剥夺( hypoxiaandglucose - deprivation ， hgd )缺血模型，首先了解了kv1 . 2蛋白的细胞定位及与vegf受体flk - 1和flt - 1的共存情况，观察了整体mcao后缺血再灌不同时间大鼠脑内kv1 . 2蛋白的磷酸化水平变化，然后通过外源性给予vegf蛋白，在sh - sy5y细胞株上观察其对缺血细胞存活率及kv1 . 2蛋白磷酸化水平的影响，最后利用vegf反义脱氧寡核苷酸( oligodeoxynucleotide ， odn )特异阻断内源性vegf蛋白的表达，观察内源性vegf蛋白在缺血细胞损伤及调节kv1 . 2蛋白磷酸化中的作用，以进一步明确vegf缺血保护效应与其调节kv1 . 2蛋白磷酸化之间的关系。