Vitexin protects against hypoxic-ischemic injury via inhibiting Ca2+/Calmodulin-dependent protein kinase II and apoptosis signaling in the neonatal mouse brain.
Vitexin protects against hypoxic-ischemic injury via inhibiting Ca2+/Calmodulin-dependent protein kinase II and apoptosis signaling in the neonatal mouse brain.
复制标题
牡荆素通过抑制新生小鼠大脑中 Ca2/钙调蛋白依赖性蛋白激酶 II 和细胞凋亡信号来防止缺氧缺血性损伤
DOI：
10.18632/oncotarget.16065
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发表时间：
2017-04-11
期刊：
影响因子：
--
通讯作者：
Peng BW
中科院分区：
文献类型：
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作者：
Min JW;Kong WL;Han S;Bsoul N;Liu WH;He XH;Sanchez RM;Peng BW
新生儿缺氧缺血是新生儿死亡和残疾的主要原因。在这项研究中，我们首次提出，牡荆素预处理可能通过抑制Ca2+/钙调蛋白依赖性蛋白激酶II的磷酸化来抑制新生儿缺氧缺血性神经元损伤中的促凋亡信号通路。在这里，我们发现牡荆素预处理以剂量依赖性方式减少脑梗塞体积。此外，牡荆素还能减少 TUNEL 阳性细胞的数量和脑萎缩。此外，牡荆素改善了神经行为结果。牡荆素还可以减少缺氧、缺糖引起的神经元损伤和钙进入。牡荆素预处理增加了 Bcl-2/Bax 蛋白比率，并降低了损伤后 24 小时 Ca2+/钙调蛋白依赖性蛋白激酶 II 和 NF-κB 的磷酸化、裂解 caspase-3 蛋白的表达。我们的数据表明，用牡荆素预处理可预防新生儿缺氧缺血性脑损伤，因此具有治疗缺氧缺血性脑损伤的潜力。
Neonatal hypoxic-ischemic is a major cause of death and disability in neonates. In this study, we suggest for the first time that pretreatment with vitexin may suppress a pro-apoptotic signaling pathway in hypoxic-ischemic neuronal injury in neonates by inhibition of the phosphorylation of Ca2+/Calmodulin-dependent protein kinase II. Here we found that vitexin pretreatment reduced brain infarct volume in a dose-dependent manner. In addition, vitexin decreased the number of TUNEL-positive cells and brain atrophy. Furthermore, vitexin improved neurobehavioral outcomes. Vitexin also reduced oxygen glucose deprivation-induced neuronal injury and calcium entry. Vitexin pretreatment increased the Bcl-2/Bax protein ratio and decreased phosphorylation of Ca2+/Calmodulin-dependent protein kinase II and NF-κB, cleaved caspase-3 protein expression 24 hours after injury. Our data indicate that pretreatment with vitexin protects against neonatal hypoxic-ischemic brain injury and thus has potential as a treatment for hypoxic-ischemic brain injury.