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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.