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Oxymatrine protects neonatal rat against hypoxic-ischemic brain damage via PI3K/Akt/GSK3β pathway

Liu, Yue, Wang, Hui, Liu, Ning, Du, Juan, Lan, Xiaobing, Qi, Xue, Zhuang, Chunlin, Sun, Tao, Li, Yuxiang, Yu, Jianqiang
Life sciences 2019
alkaloids, apoptosis, brain damage, calcium, carotid arteries, cell viability, cerebral cortex, death, glucose, hippocampus, histopathology, infarction, intraperitoneal injection, models, neonates, neurons, oxygen, phosphatidylinositol 3-kinase, pups, rats, signal transduction
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 Ca2+ 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.