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《Journal of Applied Clinical Pediatrics》 2009-12
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Effects of Glycogen Synthase Kinase-3β and Free Radical on Neuron Apoptosis of Newborn Rats with Hypoxic-Ischemic Brain Damage

DONG Wei-hua1,TAN Li-na2,GUO Xue-peng3(1.Department of Biochemistry and Molecular Biology,Xinxiang Medical University;2.Addictive Department,the Second Affiliated Hospital of Xinxiang Medical University;3.Xinxiang Medical University,Xinxiang 453003,Henan Province,China)  
Objective To study the effects of glycogen synthase kinase-3β(GSK-3β)and free radical on neuron apoptosis of hypoxic-ischemic brain damage(HIBD)in newborn rats.Methods Eighty 7-day-old neonatal rats were randomly divided into 2 groups:normal group and hypoxic-ischemic(HI)group.Rats in HI group were subjected to left common carotid artery ligation,exposed to 80 mL/L oxygen and 920 mL/L nitrogen gas in 37 ℃ closed container for 2.5 h.Rats in 2 groups were killed at 6 hours,24 hours,48 hours,72 hours,5 days after hypoxia respectively.The neuron apoptosis was detected by flow cytometry.The activity of GOD-PX and the contents of SOD and MDA were detected by spectrophotometry,the level of GSK-3β was mensurated by Enzyme-linked immumosorbent assay(ELISA).Results The rates of neuronal apoptosis in HI group were significantly higher than those in normal group at 6,24,48 and 72 hours after hypoxia,respectively(Pa0.05).The levels of neuronal apoptosis and the content of GSK-3β and MAD in HI group were significantly higher than those in normal group at 6,24,48 and 72 hours after hypoxia,respectively(Pa0.05),but the activity of GOD-PX and the content of SOD in HI group were significantly lower than those in normal group at 6,24,48 hours(Pa0.05),and the levels of neuronal apoptosis were positively correlated with GSK-3β and MAD,negatively correlated with the activity of GOD-PX and the content of SOD.Conclusions GSK-3β and free radical injury are the main mechanism of HIBD in newborn rats.The time from 24 to 72 hours is the crest-time of brain injury after brain damage.
【CateGory Index】: R722.1
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