The Influence Of Glutamate Receptor Blocker On The Apoptosis Of Hypoxic Ischemic Encephalopathy Nerve Cells

Background Hypoxic-ischemic encephalopathy(HIE) is the common disease in the perinatal period and also the main cause for the newborn’s death or disability. The ischemic and hypoxic state results in the oxygen-glucose deprivation in the nerve tissue and the serious nerve cell damage. According to the latest research, glutamate and its alpha-amino-3-hydrox-5-methyl-4-isoxazolepropionic acid(AMPA) receptor play a significant role in the occurrence and progress of HIE.The AMPA receptor expression peak forms in the23-32week fetal white brain developmental oligodendrocyte(OL). When the ischemic cerebral damage occurs in the premature infant, glutamate is over released,then the glutamate concentration in the brain rises sharply. In turn, the excessive activation of the AMPA receptor leads to the neuron’s death for the overexcitation. As a result, excitotoxicity is produced to cause widely brain pathologic damage.The research involves two menthods--in vivo animal experiment and in vitro cell cultivation to study the intervention of glutamate receptor blocker GYKI25466on the newborn rat’s nerve cell in the hypoxic-ischemic brain damage and aims at discussing the protective effect of the GYKI25466on the central lesion caused by HIE and providing experimental basis for the further research on the pathogenesis and effective prevention of HIE. Objective To discuss glutamic acid receptor blocker hypoxicischemic encephalopathy (hypoxic-ischemic encephalopathy, HIE) newborn rats cell apoptosis of inhibition. Methods In vivo: the newborn rat randomly divided into blank control group (N), hypoxicischemic brain damage group (H) and GYKI52466intervention group (G). Made the drug, observe the rat neural behavior abnormalities and ultrastructural changes. In vitro:the newborn rat’s brain cells suspension liquid made unicellular, cultivate after4days, N were given cultivating environment normal, H group of oxygen to give short of sugar environment, to lack of oxygen of group G sugar added after GYKI52466cultivating environment, after6hours each cell growth state compared, the flow cytometric analysis on brain cell apoptosis. Results In vivo:nerve behavior observation, group G and group H abnormal neural behavior than improved,by electron microscopy observation, group H of neurons nuclei structural damage, and nuclear membrane rupture, nucleoli mild shrinks, and group G structure tents to complete. In vitro:compared with model group, GYK.I52466the treatment group were far fewer cell apoptosis, numerical have extremely significant difference (P0.001).Conclusion:Glutamate receptor blocker GYK.I25466can effectively reduce the newborn rat hypoxicischemic brain damage abnormal neural behavior performance and pathology change, restrain blood anoxic nerve cells after the cell apoptosis, confirmed that GYKI25466has certain nerve protection.