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

Aims: In this study we aimed to explore the specific effect and mechanism of oxymatrine on neonatal rats hypoxic-ischemic brain damage.
Materials and Methods: 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 ²⁺ concentration, MMP and cell apoptosis were used in damage evaluation.
Key Findings: The results shown that oxymatrine regulated brain damage and cell apoptosis by controlling NR2B-PI3K/Akt/GSK3β signaling pathway.
Significance: 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.
Competing Interests: Declaration of Competing Interest The authors declare that they have no conflicts of interest.
(Copyright © 2019. Published by Elsevier Inc.)