Apoptotic Mechanisms for Neuronal Cells in Early Brain Injury After Subarachnoid Hemorrhage

被引:134
作者
Hasegawa, Yu [1 ]
Suzuki, Hidenori [1 ]
Sozen, Takumi [1 ]
Altay, Orhan [1 ]
Zhang, John H. [1 ]
机构
[1] Loma Linda Univ, Sch Med, Dept Physiol, Loma Linda, CA 92354 USA
来源
EARLY BRAIN INJURY OR CEREBRAL VASOSPASM, VOL 1: PATHOPHYSIOLOGY | 2011年 / 110卷
关键词
Apoptosis; Cerebral blood flow; Early brain injury; Intracranial pressure; Subarachnoid hemorrhage; OXYHEMOGLOBIN-INDUCED APOPTOSIS; FOCAL CEREBRAL-ISCHEMIA; C-JUN; OXIDATIVE STRESS; BLOOD-FLOW; INFLAMMATORY CYTOKINES; SODIUM ORTHOVANADATE; SUPEROXIDE-DISMUTASE; SIGNALING PATHWAYS; PERFUSION-PRESSURE;
D O I
10.1007/978-3-7091-0353-1_8
中图分类号
R74 [神经病学与精神病学];
学科分类号
100204 [神经病学];
摘要
Objects: The major causes of death and disability in subarachnoid hemorrhage (SAH) may be early brain injury (EBI) and cerebral vasospasm. Although cerebral vasospasm has been studied and treated by a lot of drugs, the outcome is not improved even if vasospasm is reversed. Based on these data, EBI is considered a primary target for future research, and apoptosis may be involved in EBI after experimental SAH. Methods: We reviewed the published literature about the relationship between SAH induced EBI and apoptosis in PubMed. Result: Most available information can be obtained from the endovascular filament perforation animal model. After onset of SAH, intracranial pressure is increased and then cerebral blood flow is reduced. Many factors are involved in the mechanism of apoptotic cell death in EBI after SAH. In the neuronal cells, both intrinsic and extrinsic pathways of apoptosis can occur. Some antiapoptotic drugs were studied and demonstrated a protective effect against EBI after SAH. However, apoptosis in EBI after SAH has been little studied and further studies will provide us more beneficial findings. Conclusions: The study of apoptosis in EBI after experimental SAH may give us new therapies for SAH.
引用
收藏
页码:43 / 48
页数:6
相关论文
共 75 条
[1]
Oxyhemoglobin as the principal cause of cerebral vasospasm: a holistic view of its actions [J].
Asano, T .
CRITICAL REVIEWS IN NEUROSURGERY, 1999, 9 (05) :303-318
[2]
Ayer RE, 2008, ACTA NEUROCHIR SUPPL, V104, P33
[3]
Bazan N G, 1980, Adv Neurol, V28, P197
[4]
Acute vasoconstriction after subarachnoid hemorrhage [J].
Bederson, JB ;
Levy, AL ;
Ding, WH ;
Kahn, R ;
DiPerna, CA ;
Jenkins, AL III ;
Vallabhajosyula, P .
NEUROSURGERY, 1998, 42 (02) :352-360
[5]
CORTICAL BLOOD-FLOW AND CEREBRAL PERFUSION-PRESSURE IN A NEW NONCRANIOTOMY MODEL OF SUBARACHNOID HEMORRHAGE IN THE RAT [J].
BEDERSON, JB ;
GERMANO, IM ;
GUARINO, L .
STROKE, 1995, 26 (06) :1086-1091
[6]
p53 may play an orchestrating role in apoptotic cell death after experimental subarachnoid hemorrhage [J].
Cahill, Julian ;
Calvert, John W. ;
Marcantonio, Suzzanne ;
Zhang, John H. .
NEUROSURGERY, 2007, 60 (03) :531-545
[7]
CHAKRABONI S, 1988, CELL SIGNAL, V10, P675
[8]
Mitochondria and neuronal death/survival signaling pathways in cerebral ischemia [J].
Chan, PH .
NEUROCHEMICAL RESEARCH, 2004, 29 (11) :1943-1949
[9]
p38 MAP kinase mediates nitric oxide-induced apoptosis of neural progenitor cells [J].
Cheng, AW ;
Chan, SL ;
Milhavet, O ;
Wang, SQ ;
Mattson, MP .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (46) :43320-43327
[10]
CHENG G, 2009, BMC NEUROSCI, DOI DOI 10.1186/14712202107