Erythropoietin prevents ischemia-reperfusion from inducing oxidative damage in fetal rat brain

被引:115
作者
Solaroglu, I
Solaroglu, A
Kaptanoglu, E [1 ]
Dede, S
Haberal, A
Beskonakli, E
Kilinc, K
机构
[1] Ankara Numune Res & Educ Hosp, Dept Neurosurg, Ankara, Turkey
[2] Ankara Matern & Womens Hlth Teaching Hosp, Dept Obstet & Gynecol, Ankara, Turkey
[3] Univ Hacettepe, Dept Biochem, Fac Med, TR-06100 Ankara, Turkey
关键词
brain; erythropoeitin; fetus; free radical; ischemia; neuroprotection;
D O I
10.1007/s00381-002-0680-2
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objective: The aim of this study was to show the effect of erythropoietin on ischemia-reperfusion-induced oxidative damage in fetal rat brain. Methods: Fetal brain ischemia was induced by clamping the utero-ovarian artery bilaterally for 20 min, and reperfusion was achieved by removing the clamps for 30 min. The control group was made up of noninjured rats that were 19 days pregnant. In the ischemia-reperfusion group no treatment was given, while 0.4 ml of human serum albumin solution and 5,000 U/kg recombinant human erythropoietin (r-Hu-EPO) were administered in the vehicle and treatment groups 30 min before ischemia-reperfusion injury. Lipid peroxidation in the brain tissue was determined as the concentration of thiobarbituric acid-reactive substances (TBARS) for each fetal rat. A one-way analysis of variance and the post-hoc test were used for statistical analysis. Results: TBARS increased to statistically significantly higher levels in fetal rat brain after ischemia-reperfusion injury than were found in the control group. Recombinant human erythropoietin prevented the increase in TBARS after ischemia-reperfusion injury. Conclusion: Recombinant human erythropoietin has been shown to have neuroprotective effect in intrauterine ischemia-reperfusion-induced fetal brain damage in rats.
引用
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页码:19 / 22
页数:4
相关论文
共 31 条
[11]  
Dame C, 2001, BIOL NEONATE, V79, P228
[12]  
DELIVORIAPAPADO.M, 1998, J PEDIATR, V132, P30
[13]   Reperfusion injury as the mechanism of brain damage after perinatal asphyxia [J].
Fellman, V ;
Raivio, KO .
PEDIATRIC RESEARCH, 1997, 41 (05) :599-606
[14]   Cytosolic and membrane-bound cerebral nitric oxide synthase activity during hypoxia in cortical tissue of newborn piglets [J].
Groenendaal, F ;
Mishra, OP ;
McGowan, JE ;
Hoffman, DJ ;
DelivoriaPapadopoulos, M .
NEUROSCIENCE LETTERS, 1996, 206 (2-3) :121-124
[15]   OXYGEN RADICALS AND THE NERVOUS-SYSTEM [J].
HALLIWELL, B ;
GUTTERIDGE, JMC .
TRENDS IN NEUROSCIENCES, 1985, 8 (01) :22-26
[16]   INHIBITOR OF NITRIC-OXIDE SYNTHESIS REDUCES HYPOXIC-ISCHEMIC BRAIN-DAMAGE IN THE NEONATAL RAT [J].
HAMADA, Y ;
HAYAKAWA, T ;
HATTORI, H ;
MIKAWA, H .
PEDIATRIC RESEARCH, 1994, 35 (01) :10-14
[17]  
HAYBERG H, 1985, J CEREB BLOOD FLOW M, V5, P413
[18]   THE EFFECT OF HIGH-DOSE ANTENATAL VITAMIN-E ON HYPOXIA-INDUCED CHANGES IN NEWBORN RATS [J].
INAN, C ;
KILIC, I ;
KILINC, K ;
KALAYCI, O ;
KOTILOGLU, E .
PEDIATRIC RESEARCH, 1995, 38 (05) :685-689
[19]   Erythropoietin receptor-mediated inhibition of exocytotic glutamate release confers neuroprotection during chemical ischemia [J].
Kawakami, M ;
Sekiguchi, M ;
Sato, K ;
Kozaki, S ;
Takahashi, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (42) :39469-39475
[20]   Oxygen free radical generation during in-utero hypoxia in the fetal guinea pig brain: the effects of maturity and of magnesium sulfate administration [J].
Maulik, D ;
Zanelli, S ;
Numagami, Y ;
Ohnishi, ST ;
Mishra, OP ;
Delivoria-Papadopoulos, M .
BRAIN RESEARCH, 1999, 817 (1-2) :117-122