EDARAVONE ALLEVIATES DELAYED NEURONAL DEATH AND LONG-DATED COGNITIVE DYSFUNCTION OF HIPPOCAMPUS AFTER TRANSIENT FOCAL ISCHEMIA IN Wistar RAT BRAINS

被引:38
作者
Jiao, L. [1 ]
Zhang, J. [1 ]
Li, Z. [1 ]
Liu, H. [1 ]
Chen, Y. [1 ]
Xu, S. [1 ]
机构
[1] Huazhong Univ Sci & Technol, Dept Neurol, Tongji Hosp, Tongji Med Coll, Wuhan 430030, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
ischemia; delayed neuronal death; cognitive dysfunction; inflammation; astrocyte; FREE-RADICAL SCAVENGER; CEREBRAL-ISCHEMIA; HYPOXIA-ISCHEMIA; OXYGEN RADICALS; DAMAGE; INJURY; RESPONSES; NEUROPROTECTION; INHIBITION; INFARCTION;
D O I
10.1016/j.neuroscience.2011.01.017
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Edaravone is currently being used in acute ischemic stroke both in clinical and experimental research as a potent antioxidant. Here we explore the effects of edaravone on delayed neuronal death (DND) and long-dated cognitive dysfunction of hippocampus after cerebral ischemia-reperfusion (IR) injury and explain the underlying mechanisms and pathways. Our findings suggested that edaravone not only significantly alleviated delayed neuronal death and cognitive dysfunction of hippocampus after cerebral focal ischemia, but also markedly decreased malondialdehyde (MDA) levels. In addition, edaravone increased superoxide dismutase (SOD) levels and reduced the levels of inflammatory cytokines such as IL-1 beta and TNF-alpha expression; edaravone, also suppressed glial fibrillary acidic protein (GFAP) proliferation at days 3, 7 and 30 after reperfusion. Overall, the consensus emerging from this body of data indicated that edaravone exerts a later neuroprotective effect to hippocampus through its ability to inhibit inflammation, suppression of astrocyte activation and scavenging free radicals in stroke events. (C) 2011 Published by Elsevier Ltd on behalf of IBRO.
引用
收藏
页码:177 / 183
页数:7
相关论文
共 28 条
[1]   STRONG ATTENUATION OF ISCHEMIC AND POSTISCHEMIC BRAIN EDEMA IN RATS BY A NOVEL FREE-RADICAL SCAVENGER [J].
ABE, K ;
YUKI, S ;
KOGURE, K .
STROKE, 1988, 19 (04) :480-485
[2]   Anti-apoptotic and neuroprotective effects of edaravone following transient focal ischemia in rats [J].
Amemiya, S ;
Kamiya, T ;
Nito, C ;
Inaba, T ;
Kato, K ;
Ueda, M ;
Shimazaki, K ;
Katayama, Y .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2005, 516 (02) :125-130
[3]   Altered neuronal and microglial responses to excitotoxic and ischemic brain injury in mice lacking TNF receptors [J].
Bruce, AJ ;
Boling, W ;
Kindy, MS ;
Peschon, J ;
Kraemer, PJ ;
Carpenter, MK ;
Holtsberg, FW ;
Mattson, MP .
NATURE MEDICINE, 1996, 2 (07) :788-794
[4]   Role of oxidants in ischemic brain damage [J].
Chan, PH .
STROKE, 1996, 27 (06) :1124-1129
[5]   Reactive oxygen radicals in signaling and damage in the ischemic brain [J].
Chan, PH .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2001, 21 (01) :2-14
[6]   Blockade of gap junctions in vivo provides neuroprotection after perinatal global ischemia [J].
de Pina-Benabou, MH ;
Szostak, V ;
Kyrozis, A ;
Rempe, D ;
Uziel, D ;
Urban-Maldonado, M ;
Benabou, S ;
Spray, DC ;
Federoff, HJ ;
Stanton, PK ;
Rozental, R .
STROKE, 2005, 36 (10) :2232-2237
[7]   FREE-RADICALS IN CEREBRAL ISCHEMIA [J].
FLAMM, ES ;
DEMOPOULOS, HB ;
SELIGMAN, ML ;
POSER, RG ;
RANSOHOFF, J .
STROKE, 1978, 9 (05) :445-447
[8]   Ischemia-induced brain damage depends on specific gap-junctional coupling [J].
Frantseva, MV ;
Kokarovtseva, L ;
Velazquez, TLP .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2002, 22 (04) :453-462
[9]   Enhanced expression of interleukin (IL)-1 and IL-6 messenger RNA and bioactive protein after hypoxia-ischemia in neonatal rats [J].
Hagberg, H ;
Gilland, E ;
Bona, E ;
Hanson, LA ;
HahnZoric, M ;
Blennow, M ;
Holst, M ;
McRae, A ;
Soder, O .
PEDIATRIC RESEARCH, 1996, 40 (04) :603-609
[10]  
Hedtjärn M, 2002, J NEUROSCI, V22, P5910