College of Pharmacy, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region 750004, PR China; College of Life Science and Technology, China Pharmaceutical University, Nanjing, Jiangsu Province, 210009, PR China.
College of Pharmacy, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region 750004, PR China.
Life Sci. 2020 Aug 1;254:116444. doi: 10.1016/j.lfs.2019.04.070. Epub 2019 May 16.
In this study we aimed to explore the specific effect and mechanism of oxymatrine on neonatal rats hypoxic-ischemic brain damage.
Hypoxia-ischemia damage model was built by ligaturing the left common carotid artery in 7-day-old rat. Rat pups in OMT group received intraperitoneal injection with oxymatrine (120 mg/kg). Oxygen glucose deprivation/reperfusion model was created in hippocampal neurons. Neurological behavioral, histopathological alteration, cell viability, intracellular Ca concentration, MMP and cell apoptosis were used in damage evaluation.
The results shown that oxymatrine regulated brain damage and cell apoptosis by controlling NR2B-PI3K/Akt/GSK3β signaling pathway.
Neonatal hypoxic-ischemic brain damage is a destructive injury that leading to death and detrimental neurological deficits. Oxymatrine is a natural alkaloid compound that can alleviate the ischemic cerebral infarction. In the study, 120 mg/kg oxymatrine decreased neuroethology damage and neuronal damage in the cerebral cortex and the hippocampus CA3. Moreover, 0.2, 1, 5 μg/ml oxymatrine improved cell survival, decreased cell apoptosis. The utilization of LY293004 (PI3K signaling pathway inhibitor) also supported that oxymatrine ameliorated neonatal hypoxic-ischemic brain damage and cell injury by controlling NR2B-PI3K/Akt/GSK3β signaling pathway.
本研究旨在探讨氧化苦参碱对新生大鼠缺氧缺血性脑损伤的具体作用及机制。
通过结扎 7 日龄大鼠左颈总动脉建立缺氧缺血损伤模型。氧化苦参碱（120mg/kg）组腹腔注射氧化苦参碱。在海马神经元中建立氧葡萄糖剥夺/再灌注模型。神经行为学、组织病理学改变、细胞活力、细胞内 Ca 浓度、MMP 和细胞凋亡用于损伤评价。
结果表明，氧化苦参碱通过调控 NR2B-PI3K/Akt/GSK3β 信号通路调节脑损伤和细胞凋亡。
新生儿缺氧缺血性脑损伤是一种破坏性损伤，可导致死亡和不良的神经功能缺陷。氧化苦参碱是一种天然生物碱化合物，可减轻缺血性脑梗死。在本研究中，120mg/kg 氧化苦参碱降低了大脑皮质和海马 CA3 区的神经行为学损伤和神经元损伤。此外，0.2、1、5μg/ml 氧化苦参碱提高了细胞存活率，减少了细胞凋亡。利用 LY293004（PI3K 信号通路抑制剂）也支持氧化苦参碱通过调控 NR2B-PI3K/Akt/GSK3β 信号通路改善新生大鼠缺氧缺血性脑损伤和细胞损伤。
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