期刊
EXPERIMENTAL NEUROLOGY
卷 272, 期 -, 页码 145-151出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2015.02.031
关键词
Subarachnoid hemorrhage; Early brain injury; Phosphatidylcholine-specific phospholipase C; Tricyclodecan-9-yl-xanthogenate
资金
- National Natural Science Foundation of China [81371279, 81422013, 81471196, 81400949]
- Jiangsu Province's Outstanding Medical Academic Leader program [LJ201139]
- Scientific Department of Jiangsu Province [BL2014045]
- Suzhou Government [LCZX201301, SZS201413, SYS201332]
- Project Funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions
Neuron apoptosis and inflammatory responses contribute to subarachnoid hemorrhage (SAH)-induced early brain injury (EBI), which is the main aspect that affects patients' outcome. Previous research has demonstrated that phosphatidylcholine-specific phospholipase C (PC-PLC) plays critical roles in cell apoptosis and various inflammatory responses, and that tricyclodecan-9-yl-xanthogenate (D609), a well known PC-PLC inhibitor, is a powerful agent to protect brain from cerebral ischemic injury and SAH-induced cerebral vasospasm. However, the association between PC-PLC and SAH-induced EBI is undetermined. Therefore, we sought to investigate whether PC-PLC was implicated in SAH-induced EBI. Compared with sham group, an upregulation of PC-PLC activity was detected in the brain tissue and serum of SAH group. Pharmacological blockade of PC-PLC by D609 attenuated neurological behavior impairment, brain edema and blood-brain barrier (BBB) damage induced by SAH. In addition, D609 treatment significantly inhibited SAH-induced inflammatory response and neuron apoptosis. Furthermore, inhibition of PC-PLC in primary-cultured rat cortical neurons attenuated oxyhemoglobin (OxyHb)-induced apoptosis morphology and decrease in survival rate. In conclusion, our data suggest that PC-PLC participates in SAH-induced EBI. (C) 2015 Elsevier Inc All rights reserved.
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